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Micronase

Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Other names for this medication:

Similar Products:
Glucophage, Actos, Glucotrol, Avandia

 

Also known as:  Glyburide.

Description

Generic Micronase is used for treating type 2 diabetes. It is used along with diet and exercise. It may be used alone or with other antidiabetic medicines.

Generic Micronase is a sulfonylurea antidiabetic medicine. It works by causing the pancreas to release insulin, which helps to lower blood sugar.

Brand name of Generic Micronase is Micronase.

Dosage

Take Generic Micronase by mouth with food.

If you are taking 1 dose daily, take Generic Micronase with breakfast or the first main meal of the day unless your doctor tells you otherwise.

High amounts of dietary fiber may decrease Generic Micronase 's effectiveness, resulting in high blood sugar.

Generic Micronase works best if it is taken at the same time each day.

Continue to take Generic Micronase even if you feel well.

If you want to achieve most effective results do not stop taking Generic Micronase suddenly.

Overdose

If you overdose Generic Micronase and you don't feel good you should visit your doctor or health care provider immediately.

Storage

Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Throw away any unused medicine after the expiration date. Keep out of reach of children.

Side effects

The most common side effects associated with Micronase are:

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Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.

Contraindications

Do not take Generic Micronase if you are allergic to Generic Micronase components.

Do not take Generic Micronase if you're pregnant or you plan to have a baby, or you are a nursing mother. Generic Micronase can ham your baby.

Do not take Generic Micronase if you have certain severe problems associated with diabetes (eg, diabetic ketoacidosis, diabetic coma).

Do not take Generic Micronase if you have moderate to severe burns or very high blood acid levels (acidosis) you are taking bosentan.

Do not take Generic Micronase if you are taking bosentan.

Be careful with Generic Micronase if you are taking any prescription or nonprescription medicine, herbal preparation, or dietary supplement.

Be careful with Generic Micronase if you have allergies to medicines, foods, or other substances.

Be careful with Generic Micronase if you have had a severe allergic reaction (eg, a severe rash, hives, itching, breathing difficulties, dizziness) to any other sulfonamide medicine, such as acetazolamide, celecoxib, certain diuretics (eg, hydrochlorothiazide), glipizide, probenecid, sulfamethoxazole, valdecoxib, or zonisamide.

Be careful with Generic Micronase if you have a history of liver, kidney, thyroid, or heart problems.

Be careful with Generic Micronase if you have stomach or bowel problems (eg, stomach or bowel blockage, stomach paralysis), drink alcohol, or have had poor nutrition.

Be careful with Generic Micronase if you have type 1 diabetes, very poor health, a high fever, a severe infection, severe diarrhea, or high blood acid levels, or have had a severe injury.

Be careful with Generic Micronase if you have a history of certain hormonal problems (eg, adrenal or pituitary problems, syndrome of inappropriate secretion of antidiuretic hormone [SIADH]), low blood sodium levels, anemia, or glucose-6-phosphate dehydrogenase (G6PD) deficiency.

Be careful with Generic Micronase if you will be having surgery.

Be careful with Generic Micronase if you are taking bosentan because liver problems may occur; the effectiveness of both medicines may be decreased; beta-blockers (eg, propranolol) because the risk of low blood sugar may be increased; they may also hide certain signs of low blood sugar and make it more difficult to notice; angiotensin-converting enzyme (ACE) inhibitors (eg, enalapril), anticoagulants (eg, warfarin), azole antifungals (eg, miconazole, ketoconazole), chloramphenicol, clarithromycin, clofibrate, fenfluramine, insulin, monoamine oxidase inhibitors (MAOIs) (eg, phenelzine), nonsteroidal anti-inflammatory drugs (NSAIDs) (eg, ibuprofen), phenylbutazone, probenecid, quinolone antibiotics (eg, ciprofloxacin), salicylates (eg, aspirin), or sulfonamides (eg, sulfamethoxazole) because the risk of low blood sugar may be increased; calcium channel blockers (eg, diltiazem), corticosteroids (eg, prednisone), decongestants (eg, pseudoephedrine), diazoxide, diuretics (eg, furosemide, hydrochlorothiazide), estrogens, hormonal contraceptives (eg, birth control pills), isoniazid, niacin, phenothiazines (eg, promethazine), phenytoin, rifamycins (eg, rifampin), sympathomimetics (eg, albuterol, epinephrine, terbutaline), or thyroid supplements (eg, levothyroxine) because they may decrease Generic Micronase 's effectiveness, resulting in high blood sugar; gemfibrozil because blood sugar may be increased or decreased; cyclosporine because the risk of its side effects may be increased by Generic Micronase.

Avoid alcohol.

Do not stop taking Generic Micronase suddenly.

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The bile salt export pump (BSEP) is the major bile salt transporter in the liver canalicular membrane. Our aim was to determine the affinity of the human BSEP for bile salts and identify inhibitors.

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Single-channel recording techniques were used to identify and characterize the K+ channel activated by Ca(2+)-mediated secretory agonists in T84 cells. Carbachol (CCh; 100 microM) and taurodeoxycholate (TDC; 0.75 mM) stimulated oscillatory outward K+ currents. With K gluconate in bath and pipette, cell-attached single-channel K+ currents stimulated by CCh and ionomycin (2 microM) were inwardly rectified and reversed at 0 mV. The single-channel chord conductance was 32 pS at -90 mV and 14 pS at +90 mV. Similar properties were observed in excised inside-out patches in symmetric K+, permitting further characterization of channel properties. Partial substitution of bath or pipette K+ with Na+ gave a K(+)-to-Na+ selectivity ratio of 5.5:1. Channel activity increased with increasing bath Ca2+ concentration in the physiological range of 50-800 nM. Maximal channel activity occurred at intracellular pH 7.2 and decreased at more acidic or alkaline pH values. Extracellular charybdotoxin (CTX; 50 nM) blocked inward but not outward currents. Extracellular tetraethylammonium (TEA; 10 mM) reduced single-channel amplitude at all voltages. No apparent block of the channel was observed with extracellular Ba2+ (1 mM), apamin (1 microM), 4-aminopyridine (4-AP; 4 mM), quinine (500 microM), or glyburide (10 microM). Cytosolic quinine and 4-AP blocked both inward and outward currents, whereas Ba2+ blocked only outward currents. Apamin, CTX, TEA, and glyburide did not affect channel activity. The agonist activation and pharmacological profile of this inwardly rectified K+ channel indicate that it is responsible for the increase in basolateral K+ conductance stimulated by Ca(2+)-mediated agonists in T84 cells.

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The effects of glibenclamide and BRL-38227 were studied in isolated rabbit hearts subjected to ischemia and programmed electrical stimulation. Coronary artery occlusion over 24 min decreased the ventricular effective refractory period in the ischemic zone. BRL-38227 (0.1 microM) showed significant coronary vasodilator effects, but failed to modify the ventricular effective refractory period under these conditions. A higher concentration (5 microM) of BRL-38227 potentiated the ischemia induced ventricular effective refractory period shortening effects. Glibenclamide (0.1 and 1 microM) delayed the onset of the ischemia-induced ventricular effective refractory period shortening. Glibenclamide (1 microM) inhibited the potentiated ventricular effective refractory period shortening effects of BRL-38227 (5 microM) during ischemia, but failed to antagonise the coronary vasodilator effects of BRL-38227 (5 microM). A higher incidence of ventricular fibrillation was inducible when an extra beat was applied in the ischemic zone through programmed electrical stimulation. The incidence of programmed electrical stimulation induced ventricular fibrillation was increased by BRL-38227 (5 microM) and antagonised by glibenclamide (1 microM). The results suggest that high concentrations of KATP-activators can accentuate ischemia-induced decreases in refractory period and increase the susceptibility of hearts to ventricular fibrillation when an extra beat is applied to the ischemic myocardium. These effects did not occur at lower coronary vasodilating concentrations of BRL-38227.

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High-resistance micro-electrodes were used to measure membrane potentials in beta-cells from islets of Langerhans of ob/ob obese mice (Norwich colony). In the presence of glucose the burst pattern of electrical activity recorded in ob/ob beta-cells, although similar to the burst pattern recorded from normal beta-cells, presents important differences. The membrane potential of the ob/ob beta-cells in the presence of 11 mM glucose in the modified Krebs solution oscillates between a silent-phase level at -48 mV and an active-phase level at -36 mV, similarly to normal mouse islet beta-cells. However, the average active-phase duration is 20 s in ob/ob beta-cells compared with 5 s in normal beta-cells. The average burst frequency is 1.8 bursts/min in ob/ob beta-cells compared with 3 bursts/min in normal beta-cells. While normal beta-cells show continuous spike activity above 16 mM glucose, ob/ob beta-cells often exhibit a burst pattern of electrical activity at glucose concentrations as high as 33 mM. Compared with normal beta-cells, the relationship between spike frequency and glucose concentration is shifted towards lower concentrations in ob/ob beta-cells. Thus, the concentration for half-maximal spike frequency is 6.9 mM for the ob/ob beta-cells and 10.2 mM for the normal beta-cells. In ob/ob beta-cells, the mitochondrial inhibitor carbonyl-cyanide m-chlorophenylhydrazone induces hyperpolarization of the membrane, consistent with its effect of stimulating K+ permeability in normal islets. However, quinine and the sulphonylurea glibenclamide did not block the silent phase between the bursts of electrical activity. Both drugs block the [Ca2+]i-activated K+ permeability thought to control the membrane potential at the silent phase in normal beta-cells. The modified pattern of response to glucose and decreased sensitivity to quinine and glibenclamide suggest that the beta-cell membrane of the ob/ob islet of Langerhans has a modified [Ca2+]i-activated K+ permeability.

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A 45-year-old man had been complaining of thirst and polydypsia for the last 3 months and was diagnosed as having type 2 diabetes mellitus because his fasting blood glucose showed 221 mg/dl with positive urinary ketone. He was hospitalized to a private hospital and Penfil 30R was started. However, serum gamma-GTP and aminotransferases began to elevate after insulin treatment and exceeded 1000 IU/l. Insulin was discontinued and serum gamma-GTP and aminotransferases returned close to the normal range. Since his glycemic control became poor again, Penfil 30R was restarted and serum gamma-GTP and aminotransferases elevated again. Therefore, insulin was discontinued and the patient was referred to the Third Department of Internal Medicine, Yamanashi Medical University Hospital because of liver dysfunction. His plasma glucose decreased by diet therapy, and improved further by the administration of glibenclamide. After obtaining informed consent, Humalin R was challenged. Seven days after insulin injection, serum aminotransferases began to elevate again. Lymphocyte stimulation test was negative against three preparations (Penfil R, Penfil N and Humalin R). The present case suggests that human insulin itself can cause liver dysfunction and we need to pay more attention to liver function tests when we start insulin treatment.

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The ATP-sensitive K+ channel controls insulin secretion from the islet. Mutations in KCNJ11 can cause permanent and transient neonatal diabetes. To date, more than 30 KCNJ11 mutations have been revealed as related to the onset of neonatal diabetes mellitus (NDM), most of which are responsive to glibenclamide treatment. In the present study, we sequenced the KCNJ11 gene in a Chinese girl diagnosed with NDM and in her parents. An in-frame 15-bp KCNJ11 deletion was identified in the patient, whereas no KCNJ11 deletions were found in her parents, indicating that this deletion was de novo. The patient was responsive to the treatment of glibenclamide. Ten months of follow-up showed that, besides permanent NDM, the motor and intelligence development of the girl was normal and she suffered no onset of convulsions. The result, to some degree, improved our knowledge on NDM.

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For this study, we investigated the changes in the electrophysiological parameters of Sertoli cells in seminiferous tubules from 17 - 19 day-old rats induced by testosterone. Using conventional intracellular microelectrode techniques, we analysed the membrane potential and its input resistance. The entire tubules were fixed in a superfusion chamber continuously perfused with Krebs-Ringer bicarbonate buffer (pH 7.4, 32 degrees C). Visual control of cell impalement was achieved using an inverted microscope. The parameters analysed were passed through an amplifier and recorded using a proprietary software system. The topical application of testosterone (0.1 to 10 microM) led to an immediate (within 30 seconds) and significant dose-dependent depolarization of the membrane potential of the cell at all concentrations used. Concomitantly, the input resistance of the cell membrane underwent a significant increment at 30 seconds. These changes returned to resting values after washout. Topical administration of 17beta-estradiol or progesterone (10 microM) did not change the membrane potential. The addition of the K +ATP channel agonist diazoxide to the perfusion buffer nullified the depolarization effect of testosterone at 30 seconds. This result suggests that the immediate action of testosterone is associated with the closing of K +ATP channels, thereby depolarizing the membrane.

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These results indicate that halothane and enflurane act to reduce the magnitude of K+ATP channel-mediated pulmonary vasodilation. Reflex pulmonary vasoconstriction resulting from K+ATP mediated systematic hypotension does not alter the magnitude of the pulmonary vasodilator response to lemakalim nor is it responsible for the attenuated response to K+ATP channel activation during halothane anesthesia.

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The effects of sulfonylureas and a biguanide on membrane-bound low Km cyclic AMP phosphodiesterase and lipolysis were examined in rat fat cells. Pharmacologically active sulfonylureas, such as tolbutamide (10 mM), acetohexamide (10 mM) and glibenclamide (200 microM) activated the phosphodiesterase when incubated with fat cells and suppressed lipolysis induced by isoproterenol. However, neither of these actions was observed in the presence of a pharmacologically inactive sulfonylurea, carboxytolbutamide (10 mM) and a biguanide, buformin (500 microM). Tolbutamide (0.5-10 mM) activated the enzyme, concentration dependently, and this manner of activation appears to coincide with that of the suppressive effect on the lipolysis. The time course of the enzyme activation was similar to that seen with insulin. Km, optimal pH and sensitivity to temperature of the enzyme from tolbutamide-treated cells were the same as those of the enzyme from control and insulin-treated cells. Direct incubation of the enzyme from control cells with tolbutamide did not affect the activity, while as little as 10 microM 3-isobutyl-1-methylxanthine markedly inhibited the enzyme. Tolbutamide continued to activate the enzyme in cells in which insulin receptor had been destroyed by trypsin-pretreatment. These results are compatible with the idea that the enzyme activated by sulfonylurea and that activated by insulin may be the same species of phosphodiesterase and that the antilipolytic action of sulfonylurea may be mediated by the activation of the enzyme which does not occur through the insulin receptor.

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For glibenclamide bioavailability studies in serum, high-performance liquid column and thin-layer chromatographic methods were introduced. Both methods are specific, accurate and sensitive with detection limits of at least 5 ng of glibenclamide per ml of serum. Detection is performed in the ultraviolet at wavelengths of 200 nm for liquid chromatography or 300 nm for thin-layer chromatography. Serum levels determined by either method correlated well with those determined by an already existing radioimmunoassay. Some pharmacokinetic data were computed using a one-compartment open model.

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The relationship between insulin action and control of the adipocyte-derived factor adiponectin was studied in age- and weight-matched obese individuals with type 2 diabetes failing sulfonylurea therapy. After initial metabolic characterization, subjects were randomized to troglitazone or metformin treatment groups; all subjects received glyburide (10 mg BID) as well. Treatment was continued for 3 months. The extent of glycemic control after treatment was similar in both groups. However, the increase in maximal insulin-stimulated glucose disposal rate was greater following troglitazone therapy (+44%) compared with metformin treatment (+20%). Troglitazone treatment increased serum adiponectin levels nearly threefold. There was no change in serum adiponectin with metformin treatment. A positive correlation was found between increases in whole-body glucose disposal rates and serum adiponectin levels after troglitazone; no such relationship was seen with metformin. The adiponectin protein content of subcutaneous abdominal adipocytes was increased following troglitazone treatment and unchanged after metformin. Adiponectin release from adipocytes was also augmented with troglitazone treatment. Adiponectin was present in adipocytes and plasma in several multimeric forms; a trimer was the major form secreted from adipocytes. These results indicate that increases in adiponectin content and secretion are associated with improved insulin action but are not directly related to glycemic control. Modulation of adipocyte function, including upregulation of adiponectin synthesis and secretion, may be an important mechanism by which thiazolidinediones influence insulin action.

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The results suggest that propofol induced concentration-dependent relaxations in precontracted isolated SO rings. These relaxations are independent from NO, cyclooxygenase metabolites, and opened ATP-sensitive and voltage-dependent potassium channels. Opened Ca(2+)-sensitive K(+) channels and inhibited L-type Ca(2+) channels existing in smooth muscle by propofol can contribute to these relaxations. Propofol can be beneficial as alternative drugs for obtaining selective relaxation during SO manometry after controlled clinical studies.

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We have studied the impact of a previous meal on insulin and glucose responses to the subsequent administration of glibenclamide. Healthy volunteers and NIDDM patients ingested a standard low-carbohydrate breakfast, and glibenclamide was administered 110-120 min later either as an intravenous bolus (12.5 micrograms/kg body wt), or as a tablet (5 mg HB 419). When glibenclamide was administered i.v. the drug raised insulin and lowered blood glucose levels, and previous breakfast potentiated these effects both in healthy volunteers and in NIDDM patients. Conversely when glibenclamide was given as a tablet the drug per se raised C-peptide and lowered blood glucose levels under fasting conditions, whereas the drug had no effect when ingested after breakfast. Measurements of glibenclamide in plasma revealed that previous breakfast delayed the systemic appearance of ingested glibenclamide. We conclude that nutrients sensitize insulin-releasing cells to subsequent stimulation by glibenclamide, thereby aggravate a blood-glucose-lowering effect of the drug. However this effect, which could potentially induce undesirable hypoglycaemia in sulphonylurea-treated diabetics, is counteracted when glibenclamide is taken orally because of a meal-induced decrease in drug absorption.

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The sulfonylurea glibenclamide is a relatively potent inhibitor of the CFTR Cl(-) channel. This inhibition is thought to be via an open channel block mechanism. However, nothing is known about the physical nature of the glibenclamide-binding site on CFTR. Here we show that mutations in the pore-forming 6th and 12th transmembrane regions of CFTR affect block by intracellular glibenclamide, confirming previous suggestions that glibenclamide enters the pore in order to block the channel. Two mutations in the 6th transmembrane region, F337A and T338A, significantly weakened glibenclamide block, consistent with a direct interaction between glibenclamide and this region of the pore. Interestingly, two mutations in the 12th transmembrane region (N1138A and T1142A) significantly strengthened block. These two mutations also abolished the dependence of block on the extracellular Cl(-) concentration, which in wild-type CFTR suggests an interaction between Cl(-) and glibenclamide within the channel pore that limits block. We suggest that mutations in the 12th transmembrane region strengthen glibenclamide block not by directly altering interactions between glibenclamide and the pore walls, but indirectly by reducing interactions between Cl(-) ions and glibenclamide within the pore. This work demonstrates that glibenclamide binds within the CFTR channel pore and begins to define its intrapore binding site.

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This was a single-center, open-label, phase I, drug interaction study of topiramate (150 mg/day) and glyburide (5 mg/day alone and concomitantly) in patients with T2DM. The study consisted of 14-day screening, 48-day open-label treatment, and a 7-day follow-up phase. Serial blood and urine were obtained and analyzed by liquid chromatography coupled mass spectrometry/mass spectrometry for topiramate, glyburide, and its active metabolites M1 (4-trans-hydroxy-glyburide) and M2 (3-cis-hydroxy-glyburide) concentrations. Pharmacokinetic parameters were estimated by model-independent methods. Changes in fasting plasma glucose from baseline and safety parameters were monitored throughout the study.

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Isolated rat middle cerebral arteries were perfused and superfused with physiological salt solution equilibrated with a control (approximately 140 mmHg) or reduced (approximately 35-40 mmHg) PO2. In other experiments, cerebral arteries were isolated and prostacyclin release was determined by radioimmunoassay for 6-ketoprostaglandin F1alpha. Equilibration of the vessels with reduced PO2 (35 mmHg) solution caused a significant increase in prostacyclin release relative to control PO2 (140 mmHg) conditions. Exposure of middle cerebral arteries to reduced PO2 caused vascular smooth muscle (VSM) hyperpolarization and vessel relaxation, which could be blocked by 1 microM glibenclamide, an inhibitor of the ATP-sensitive K+ channel, but not by 1 mM tetraethylammonium (TEA), an inhibitor of the Ca2+-activated K+ channel. Glibenclamide also inhibited VSM hyperpolarization and vasodilation in response to the stable prostacyclin analog iloprost, but TEA did not affect iloprost-induced dilation of the vessel. Endothelial removal eliminated the electrical and mechanical responses of the arteries to reduced PO2, but vessel responses to iloprost were similar to those of intact vessels. The results of this study are consistent with the hypothesis that hypoxic dilation of rat middle cerebral arteries is due to VSM hyperpolarization mediated by prostacyclin-induced activation of glibenclamide-sensitive K+ channels.

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Rosiglitazone improved both plasma glucose and blood pressure levels, probably by attenuation of hyperinsulinemia and sympathetic activity, while Glibenclamide worsened blood pressure control possibly by elevation of insulin levels and activation of the sympathetic system.

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Mean daily doses and blood glucose measurements (fasting blood glucose, random blood glucose, hemoglobin A1C) were stratified in 3-month periods from the time the drug therapy was started or the patient first presented to the clinic for a total of 18 months. Long-term glycemic control was defined as fasting blood glucose less than 8.33 mmol/L (150 mg/dL).

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Non-insulin-dependent diabetes mellitus (NIDDM) is normally treated by oral hypoglycaemic agents, but their use is excluded during pregnancy because of their potential teratogenic and hypoglycaemic effects on the fetus. This caveat was recently questioned as glyburide was shown to cross an isolated cotyledon in vitro in insignificant amounts. In the present study, placental transport of glyburide in vivo was examined as an indispensable step towards clinical trials. Tritiated glyburide, C14 albumin or C14-labelled diazepam were injected into 13, 9 and 11 pregnant rats, respectively and the radioactivity was measured thereafter in maternal blood and in whole fetal extracts. The ratios between radioactivity in fetal tissue to that in maternal blood for glyburide (0.535 +/- 0.068) were similar to those of diazepam (0.641 +/- 0.057) which readily crosses the placenta. However, they differed significantly from those for albumin (0.048 +/- 0.0004) which does not cross. Moreover, glyburide in fetal tissue consistently reflected its concentration in maternal blood when measured at consecutive intervals after intravenous injection in the mother. In contrast, albumin in fetal tissue was low at all time points regardless of its levels in maternal blood when measured at different times after injection. These data suggest that glyburide crosses the placenta of pregnant rats and should therefore be considered with caution as a hypoglycaemic agent in the treatment of gestational diabetes.

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We investigated whether substance P modulates pacemaker currents generated in cultured interstitial cells of Cajal of murine small intestine using whole cell patch-clamp techniques at 30 degrees C. Interstitial cells of Cajal generated spontaneous inward currents (pacemaker currents) at a holding potential of -70 mV. Tetrodotoxin, nifedipine, tetraethylammonium, 4-aminopyridine, or glibenclamide did not change the frequency and amplitude of pacemaker currents. However, divalent cations (Ni2+, Mn2+, Cd2+, and Co2+), nonselective cationic channel blockers (gadolinium and flufenamic acid), and a reduction of external Na+ from normal to 1 mM inhibited pacemaker currents indicating that nonselective cation channels are involved in their generation. Substance P depolarized the membrane potential in current clamp mode and produced tonic inward pacemaker currents with reduced frequency and amplitude in voltage clamp mode. [D-Arg1, D-Trp7,9, Leu11] substance P, a tachykinin NK1 receptor antagonist, blocked these substance P-induced responses. Furthermore, [Sar9, Met(O2)11] substance P, a specific tachykinin NK1 receptor agonist, depolarized the membrane and tonic inward currents mimicked those of substance P. Substance P continued to produce tonic inward currents in external Ca2+-free solution or in the presence of chelerythrine, a protein kinase C inhibitor. However, substance P-induced tonic inward currents were blocked by thapsigargin, a Ca2+-ATPase inhibitor in the endoplasmic reticulum or by an external 1 mM Na+ solution. Our results demonstrate that substance P may modulate intestinal motility by acting on the interstitial cells of Cajal by activating nonselective cation channels via the release of intracellular Ca2+ induced by tachykinin NK1 receptor stimulation.

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The results showed that glibenclamide-pregnenolone had greater hypoglycemic activity than glibenclamide or glibenclamide-OH. The data also showed that the biodistribution of Tc-99m-glibenclamide-OH in all organs was less than that of the Tc-99m-glibenclamide-pregnenolone derivative.

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Right atrial sections from four patient groups-non-diabetic, insulin-dependent diabetes mellitus (IDDM), non-insulin-dependent diabetes mellitus (NIDDM) receiving glibenclamide, and NIDDM receiving metformin-were subjected to one of the following protocols: aerobic control, simulated ischemia/reoxygenation, ischemic preconditioning before ischemia, and pharmacological preconditioning with alpha 1 agonist phenylephrine, adenosine, the mito-K(ATP) channel opener diazoxide, the protein kinase C (PKC) activator phorbol-12-myristate-13-acetate (PMA), or the p38 mitogen-activated protein kinase (p38MAPK) activator anisomycin. Cellular damage was assessed using creatine kinase leakage and 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT) reduction. In mitochondrial preparations from non-diabetic and diabetic myocardium, mitochondrial membrane potential (Psi(m)) was assessed using JC-1 dye, and production of reactive oxygen species was determined.

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Increased endogenous glucose production (EGP) is a hallmark of type 2 diabetes mellitus. While there is evidence for central regulation of EGP by activation of hypothalamic ATP-sensitive potassium (K(ATP)) channels in rodents, whether these central pathways contribute to regulation of EGP in humans remains to be determined. Here we present evidence for central nervous system regulation of EGP in humans that is consistent with complementary rodent studies. Oral administration of the K(ATP) channel activator diazoxide under fixed hormonal conditions substantially decreased EGP in nondiabetic humans and Sprague Dawley rats. In rats, comparable doses of oral diazoxide attained appreciable concentrations in the cerebrospinal fluid, and the effects of oral diazoxide were abolished by i.c.v. administration of the K(ATP) channel blocker glibenclamide. These results suggest that activation of hypothalamic K(ATP) channels may be an important regulator of EGP in humans and that this pathway could be a target for treatment of hyperglycemia in type 2 diabetes mellitus.

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We report a patient with diabetes mellitus who suffered severe falciparum malaria complicated by profound and persistent hypoglycaemia. The hypoglycaemia evolved before therapy with quinine was begun and resolved with eradication of the parasitaemia. The patient reverted to her baseline hyperglycaemia despite continuation of quinine. This case illustrates the critical role of falciparum malaria in the pathogenesis of malaria-associated hypoglycaemia, rather than quinine-mediated mechanisms. Anticipation of hypoglycaemia in falciparum malaria and its vigorous treatment may improve the poor prognosis associated with this complication.

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1. This study was designed to determine whether clofilium exhibits antifibrillatory activity in a pinacidil + hypoxia-induced model of ventricular fibrillation (VF) in Langendorff-perfused hearts. 2. Ten minutes after exposure to vehicle or clofilium (0.1, 1.0 and 10.0 microM), hearts were exposed to pinacidil (1.25 microM), then subjected to 12 min of hypoxia and reoxygenated. Onset to VF was recorded. Additional groups of hearts were pretreated with UK-68,798 (1.0, 3.0 and 10.0 microM), a delayed rectifier channel blocker, and 5-hydroxydecanoate (10 microM), a known ATP-dependent K+ channel blocker, and subjected to an identical protocol. 3. Clofilium decreased the incidence of VF in a concentration-dependent manner; 7/9 control hearts developed VF vs 1/9 hearts (P = 0.007, Fisher's Exact) treated with 10.0 microM clofilium. In addition, 5-hydroxydecanoate protected hearts from VF, while UK-68,798 pretreatment did not. 4. In a separate group of hearts, electrically-induced VF was converted to sinus rhythm in 10/11 hearts after clofilium was introduced as a bolus. 5. Clofilium is capable of preventing VF in the rabbit isolated heart in a concentration-dependent manner. We have data to suggest that the ability of clofilium to attenuate the effects of pinacidil+hypoxia in our model may include blockade of metabolically active K+ channels, i.e., KATP (glibenclamide-sensitive) channel.

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Diazoxide caused an increase in 86Rb+ efflux from the rat aorta and portal vein and inhibited spontaneous activity of the latter at concentrations 100 times higher than the K+ channel opener cromakalim. In the rabbit aorta both drugs inhibited vasoconstrictor responses to angiotensin II, noradrenaline and low concentrations (less than or equal to 30 mM) of KCl in a similar manner, the antivasoconstrictor activities being abolished in vessels depolarized with greater than or equal to 35 mM K+. In vivo cromakalim was about 100 times more potent than diazoxide at lowering blood pressure in rats. Diazoxide (30 mg/kg) caused a more than 2-fold increase in plasma glucose in rats and prevented any return toward base line within 1.5 hr after a glucose load. Cromakalim had minimal effects upon glucose homeostasis at equihypotensive doses. Glibenclamide, a potent blocker of ATP-dependent K+ channels, inhibited the stimulation by cromakalim and diazoxide of 86Rb+ efflux from the portal vein and aorta (IC50 approximately 0.1 microM), antagonized their vasorelaxant effects in vitro and in vivo (20-30 mg/kg i.v.) and reversed the diazoxide-induced changes in plasma glucose and insulin levels. These results provide evidence that diazoxide, like cromakalim, is able to open 86Rb+-permeable K+ channels in vascular smooth muscle. This action is likely to be responsible for the in vitro and in vivo vasodilator activity of these two drugs. However, there would seem to be pharmacological differences between the K+ channels affected by these drugs in vascular smooth muscle and the (ATP-sensitive) K+ channels of pancreatic beta-cells, which are thought to be responsible for the effects of diazoxide on plasma glucose.

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Glibenclamide and glimepiride are potential ligands of FXR and modulate activation and signaling.

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United States, United Kingdom, and Australia.

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Vascular complications are a common factor determining morbidity and mortality of diabetic patients. In vitro studies have revealed that gliclazide has antiplatelet activities. To clinically assess this action, we measured the effects of gliclazide on platelet activities and abnormal fibrinolysis in patients with type 2 diabetes mellitus. We studied 14 patients aged 38 to 72 years (9 men and 5 women) with type 2 diabetes mellitus who have been treated with glibenclamide in our hospital for more than 6 months. We switched from glibenclamide to gliclazide using the average ratio of the respective doses, 2.5 vs 40 mg. We titrated the dose of gliclazide to keep the glycemic control at the same level as the previous (glibenclamide) treatment. We measured 10 micromol/L serotonin-induced or 0.5 micromol/L adenosine diphosphate (ADP)-induced platelet aggregate formation by particle counting using light scattering at baseline and up to 6 months after the switch. After switching to gliclazide, platelet aggregate formation induced by serotonin was significantly reduced (P < .05, compared with the levels observed after glibenclamide treatment). The body mass index, fasting plasma glucose, immunoreactive insulin, homeostasis model assessment of insulin resistance, hemoglobin A(1c) (HbA(1c)), total cholesterol, triglycerides, high-density lipoprotein cholesterol, prothrombin time, activated partial thromboplastin time, fibrinogen, thrombin-antithrombin III complex, plasmin-alpha2-plasmin inhibitor complex, and plasma plasminogen activator inhibitor type 1 (PAI-1) were not changed. In the group with improved HbA(1c) (n = 5), ADP-induced platelet aggregate formation and plasma PAI-1 level were significantly reduced (P < .05, compared with the group with aggravated HbA(1c), n = 9). Multiple regression analysis showed that percentage change of ADP-induced platelet aggregate formation (standardized beta = 0.540, P < .05) was independently associated with percentage change of plasma PAI-1 level in addition to percentage change of HbA(1c) (standardized beta = 0.657, P < .05) (R = 0.939, P < .05) after switching to gliclazide. The other independent variants, like the final dose of gliclazide, homeostasis model assessment of insulin resistance, percentage change of prothrombin time, activated partial thromboplastin time, and total cholesterol, were not significantly associated with the percentage change of plasma PAI-1 level. These results indicate that gliclazide inhibits platelet aggregation via the serotonin pathway, independently of the metabolic control per se. Furthermore, in the patients with improved glycemic control, gliclazide could inhibit ADP-induced platelet aggregation and reduce PAI-I level. Taken together, the results show that gliclazide may be more useful for the prevention of diabetic vascular complications than glibenclamide.

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micronase drug form 2016-06-24

Twelve healthy male subjects were included in this double-blind cross-over study and received a single 1.75-mg dose of glibenclamide on the 8th day of continuous administration of either placebo (reference) or voglibose 5 mg t.i.d. (test). Blood samples were taken to determine the pharmacokinetic characteristics of glibenclamide and the test/reference ratios were evaluated buy micronase according to bioequivalence criteria. Additional blood samples were taken to measure serum glucose on the same day.

micronase drug interactions 2015-01-25

Following an open-label, lead-in phase to optimize the dosing of glyburide/metformin tablets, 365 patients randomly received buy micronase additive therapy comprising rosiglitazone (4 mg once daily) or placebo for 24 weeks. Based on glycemic response, rosiglitazone dose was maintained or increased to 4 mg twice daily. Glyburide/metformin dose was maintained or reduced by 2.5/500 mg for symptomatic hypoglycemia. The primary endpoint was the change in HbA1C level from baseline to week 24. The proportions of patients achieving HbA1C levels <7% and a fasting plasma glucose level <126 mg/dL were also assessed.

micronase generic name 2017-03-01

Helodermin-caused vascular relaxation was simultaneously measured with intracellular Ca2+ concentration ([Ca2+]i) in rat mesenteric artery. Helodermin caused concentration-dependent relaxation in the mesenteric artery preconstricted with norepinephrine (NE). Helodermin-caused relaxation was accompanied by decrease in [Ca2+]i, D-cis-Diltiazem, a Ca2+ channel blocker, also lowered the [Ca2+]i and tension increased by NE. However, helodermin relaxed the artery more efficiently than D-cis-diltiazem, suggesting that the peptide decreased myofilament Ca2+ sensitivity. The vascular relaxation and the corresponding decrease in [Ca2+]i induced by helodermin were partly, but significantly attenuated by glibenclamide. Helodermin-induced vascular responses were mimicked by vasoactive intestinal polypeptide (VIP) or forskolin. Furthermore, helodermin increased cAMP contents in the mesenteric artery. These findings show that vasodilatation induced by helodermin is attributable to lowered [Ca2+]i of arterial smooth muscle partly buy micronase through the activation of glibenclamide-sensitive K+ channels, and to decrease in the myofilament Ca2+ sensitivity. The increase in the cellular cAMP content probably plays a key role in the peptide-induced vasorelaxation.

micronase cost 2016-04-05

ATP-sensitive potassium (K(ATP)) channel openers have been shown to protect against cellular damage in neurons, cardiac muscle, and kidney and to effectively reduce nonsteroidal anti-inflammatory drug (NSAID)-induced gastric damage in rats. We investigated the effects of K(ATP) channel opener diazoxide on small intestinal injury induced in rats by indomethacin administration. The effect of glibenclamide, a K(ATP) channel blocker, was also evaluated. Diazoxide (15, 45 and 135mg/kg) or glibenclamide (18mg/kg), were given by oral gavage 1h before and 6h after indomethacin treatment (20mg/kg p.o.). After 24h, macroscopic and histologic lesions, myeloperoxidase (MPO) activity and lipid peroxidation levels were evaluated. Diazoxide at 15mg/kg was ineffective, while at doses of 45mg/kg and 135mg/kg was able to significantly improve all damage parameters. Glibenclamide administration enhanced intestinal injury. These results show for the first time a beneficial buy micronase effect of diazoxide in indomethacin-induced enteritis in the rat. Several mechanisms, such as oxidative phosphorylation uncoupling and hypermotility seem particularly important in NSAID-induced intestinal injury. Such events lead to increased mucosal permeability and to penetration of noxious lumen components, which ignite the inflammatory response. Since K(ATP) channel openers were shown to protect against mitochondrial damage, to reduce intercellular permeability and to relax smooth muscle, we suggest that diazoxide could exert its beneficial effects by one or more of these actions.

micronase drug class 2017-09-26

The therapeutic effect of TCM-WM was better than that buy micronase of WM.

micronase 10 mg 2017-06-12

Insulin tolerance test was done to assess the insulin sensitivity in a group of untreated non insulin dependent diabetic subjects before and after sulfonylurea (tolbutamide, glibenclamide, glipizide) therapy. The parameters buy micronase studied were KITT, slope of the blood glucose fall, summation values, and area under the curve of glucose response. All the three commonly used sulphonylurea drugs improved insulin sensitivity after 4 weeks of therapy.

micronase 5 mg 2016-07-13

1. We determined the contributions of three independent vasodilator mechanisms (cyclo-oxygenase metabolites, nitric oxide and ATP-sensitive potassium channels) in the mediation of pulmonary vasomotor effects of endothelin-1 (ET-1) in neonatal pigs. 2. Lungs of piglets (2.7 +/- 0.3 days old) were perfused at constant flow (60 ml min-1) with recirculating Ringer-albumin solution. We measured pulmonary artery pressure (Ppa) and the distribution of pulmonary vascular resistance using the double-occlusion method. 3. ET-1 (10(-12)-10(-9) M) produced concentration-dependent pulmonary vasodilatation. ET-1 (10(-9) M) decreased Ppa from 24.5 +/- 3.1 to 17.0 +/- 3.0 cmH2O with a nadir occurring at 1 min, followed by a slow return to baseline over 60 min (time for half-recovery (t1/2R) of 17.2 min). The decrease in Ppa was the result of pulmonary precapillary vasodilatation. Endothelin-3 (ET-3) (10(-12) and 10(-11) M) also induced vasodilatation comparable to equimolar concentrations of ET-1, whereas the selective ETB receptor agonist IRL 1620 at equimolar concentrations caused a more protracted vasodilatation response. 4. Neither the cyclo-oxygenase inhibitor indomethacin (10(-5) M) nor the KATP+ (ATP-sensitive) potassium channel blocker glibenclamide (10(-5) M) significantly altered the baseline Ppa; moreover, neither inhibitor affected the ET-1-induced vasodilatation, indicating the lack of involvement of cyclo-oxygenase metabolites and KATP+ channel activity in the mediation of the pulmonary vasodilator response to ET-1. 5. Addition of 10(-5) M reduced haemoglobin, which antagonizes the action of nitric oxide (NO), increased Ppa over prehaemoglobin levels. Haemoglobin significantly decreased the duration (t1/2R, 3.8 +/- 0.7 min) of pulmonary vasodilatation to ET-1, but did not abolish the initial phase of the response. L-N-Monomethylarginine, an inhibitor of NO synthesis, either alone or in combination with haemoglobin, similarly reduced the duration of ET-1-induced pulmonary vasodilatation. 6. The ETA receptor antagonist [Dpr1-Asp15]-ET-1 (Dpr, diaminoproprionic acid) had no buy micronase effect on pulmonary vasodilatation induced by ET-1, ET-3 or IRL 1620 (suc-(Glu9,Ala11,15)-ET-1(8-21)). This finding combined with the observed relative potencies of the peptides (IRL 1620 > ET-1 = ET-3) suggests that pulmonary vasodilatation was mediated by activation of the non-selective ETB receptor. 7. The results indicate that the sustained ET-1-induced pulmonary vasodilatation in neonates is probably mediated via ETB receptor activation and that it is critically dependent on NO.

micronase dosage 2016-03-30

The effects of BRL 34915, a newly developed potassium channel opener, on renal hemodynamics and function were investigated in anesthetized dogs. An i.v. injection of BRL 34915 (4, 20 and 100 micrograms/kg) caused a dose-related reduction of mean arterial pressure but there were no significant changes in renal blood flow. The agent at lower doses (4 and 20 micrograms/kg) produced a slight increasing action on urine formation. When BRL 34915 was infused intrarenally at nonhypotensive doses (0.04 and 0.2 micrograms/kg/min), there were no significant increases in renal blood flow and glomerular filtration rate. At 1.0 micrograms/kg/min, a dose which produced a slight reduction in mean arterial pressure, significant decreases in calculated renal vascular resistance were observed, thereby indicating that BRL 34915 has vasodilator action on the renal vasculature. In cases of infusion at higher doses (0.2 and 1.0 micrograms/kg/min), the levels of urine flow, urinary excretion of sodium and fractional excretion of sodium were elevated significantly and these events were accompanied by decreases in urine osmolality. Although the intrarenal buy micronase administration of BRL 34915 at higher doses produced no alterations in the fractional excretion of lithium (index of sodium excretion at the proximal tubules), the agent did increase the calculated value of the fractional distal excretion of sodium. These effects seen when BRL 34915 was infused intrarenally were suppressed markedly by glibenclamide (6 mg/kg i.v.), a putative inhibitor of the ATP-sensitive potassium channel. Our results suggest that BRL 34915 has renal vasodilating and diuretic effects as a result of opening the potassium channels within the kidney. The agent-induced diuresis may be due partly to an inhibitory effect on sodium reabsorption at the distal portion of the tubules beyond the proximal tubules.

micronase 50 mg 2016-12-22

Voglibose did not interact buy micronase with glibenclamide on a pharmacokinetic level. Concomitant treatment was well tolerated and has been proven to be safe for further clinical use.

micronase dosing 2017-01-20

It has been found that nicorandil can attenuate myocardial no-reflow. However, the exact cause of this beneficial effect has remained unclear. We investigated whether the beneficial effect of nicorandil on myocardial no-reflow could be buy micronase partly due to its protection against endothelial dysfunction.

dosage of micronase 2016-08-21

Recent studies have clarified that rates of neonatal mortality and congenital malformations are not higher among the offspring of mothers with GDM. Treatment might affect birth weight, but whether treatment is associated with reductions in rates of shoulder dystocia and cesarean section is unclear. Several level I studies conclude that the oral hypoglycemic glyburide can be used safely and effectively buy micronase during the second and third trimesters of pregnancy.

micronase medication 2017-12-27

ATP-sensitive potassium channels (KATP) open during myocardial ischemia. The ensuing repolarising potassium efflux shortens the action potential. Accumulation of extracellular potassium is able to partially depolarise the membrane, reducing the upstroke velocity of the action potential and thereby impairing impulse conduction. Both mechanisms are believed to be involved in the development of reentrant arrhythmias during cardiac ischemia. The sulfonylthiourea HMR 1883 (1-[[5-[2-(5-chloro-O-anisamido)ethyl]-methoxyphenyl]sulfonyl]-3-m ethylthiourea) was designed as a cardioselective KATP channel blocker for the prevention of arrhythmic sudden death in patients with ischemic heart disease. The aim of this study was to show that this compound, which has already shown antifibrillatory efficacy in dogs and rats, is able to inhibit ischemic changes of the action potential induced by coronary artery occlusion in anesthetised pigs. Action potentials were taken in situ with the technique of monophasic action potential (MAP) recording. In a control group (n=7), three consecutive occlusions of a small branch of the left circumflex coronary artery resulted in reproducible reductions in MAP duration and a decrease in upstroke velocity. In a separate group (n=7), HMR 1883 (3 mg/kg i.v.) significantly (P<0.05) reduced the ischemia-induced shortening of the MAP: during the first and second control occlusion of the coronary artery in the HMR 1883-group, MAP50 duration shortened from 218.5 +/- 3.0 ms to 166.7 +/- 3.3 ms and from 219.7 +/- 4.5 ms to 164.9 +/- 1.8 ms, respectively. After HMR 1883, during the third occlusion, MAP duration decreased from 226.9 +/- 3.6 ms to 205.3 +/- 4.3 ms only corresponding to 59% inhibition. HMR 1883 also improved the upstroke velocity of the MAP, which was depressed by ischemia: in the two preceding control occlusions ischemia prolonged the time to peak of the MAP, an index for upstroke velocity, from 10.83 +/- 0.43 ms to 39.42 +/- 1.60 ms and from 12.97 +/- 0.40 ms to 37.17 +/- 2.98 ms, respectively. With HMR 1883, time to peak during ischemia rose from 12.42 +/- 0.51 ms to 25.53+/-2.51 ms only, corresponding to an average inhibitory effect of 53.4%. The irregular repolarisation contour of the ischemic MAP was also improved. In conclusion, the present results indicate that HMR 1883 effectively blocks myocardial KATP channels during coronary buy micronase ischemia in anesthetised pigs, preventing an excessive shortening of the action potential and improving excitation propagation.

micronase buy cheap 2016-04-08

A retrospective database analysis compared costs among patients with type 2 diabetes buy micronase receiving four antidiabetic regimens: (1) repaglinide monotherapy, (2) metformin monotherapy, (3) repaglinide and metformin in combination, or (4) metformin and glyburide in combination. Pharmacy, medical, and total costs were measured for each cohort over a nine-month period. Although not statistically significant, total adjusted costs were lowest for the repaglinide-metformin combination ($8,924), followed by metformin monotherapy ($9,448), metformin and glyburide ($9,576), and repaglinide monotherapy ($11,910). These results must be confirmed in larger populations, but they imply that differences in pharmacy costs of repaglinide-metformin therapy are offset by measurable medical cost savings.

micronase tablets 2015-01-10

In this study, evidence is given that a number of isolated coupled plant mitochondria (from durum wheat, bread wheat, spelt, rye, barley, potato, and spinach) can take up externally added K(+) ions. This was observed by following mitochondrial swelling in isotonic KCl solutions and was confirmed by a novel method in which the membrane potential decrease due to externally added K(+) is measured fluorimetrically by using safranine. A detailed investigation of K(+) uptake by durum wheat mitochondria shows hyperbolic dependence on the ion concentration and specificity. K(+) uptake electrogenicity and the non-competitive inhibition due to either ATP or NADH are also shown. In the whole, the experimental findings reported in this paper demonstrate the existence of the mitochondrial K(+)(ATP) channel in plants (PmitoK(ATP)). Interestingly, Mg(2+) and glyburide, which can inhibit mammalian K(+) channel, have no effect on PmitoK(ATP). In the presence of buy micronase the superoxide anion producing system (xanthine plus xanthine oxidase), PmitoK(ATP) activation was found. Moreover, an inverse relationship was found between channel activity and mitochondrial superoxide anion formation, as measured via epinephrine photometric assay. These findings strongly suggest that mitochondrial K(+) uptake could be involved in plant defense mechanism against oxidative stress due to reactive oxygen species generation.

micronase brand name 2015-10-29

The present work describes a simple method for direct drug administration into Zovirax Drug Classification the dorsal root ganglion (DRG) in anesthetized rats. This technique does not involve surgery, is easy to learn and allows behavioral testing within minutes after the injection. Based on landmarks that target the L5 DRG, an orifice was created with a guide needle through which a specially designed needle was inserted for solution injection. Its introduction into the ganglia was ensured by the triggering of an ipsilateral hindpaw reflex. The precision of the technique was checked by injections of the biological dye Pontamine Sky Blue (PSB) or C14-labeled arginine. There was no leakage of the dye to the surrounding tissues after a single 4 microl or three successive 2.5 microl injections (at 30-min intervals). Moreover, identical effects were observed with prostaglandin E2 (PGE2), morphine or glibenclamide injected intraplantarly or in the DRG, thus confirming the precision of the method and suggesting that the ganglion cells and peripheral nociceptors may display similar receptor population.

micronase drug information 2015-11-18

Patient compliance and treatment satisfaction with once Clomid And Alcohol -daily glimepiride were significantly better than with glibenclamide 2 to 3 times daily.

micronase drug form 2016-08-18

Human erythrocytes infected with Plasmodium falciparum have markedly increased permeability to diverse solutes, many of which may be mediated by an unusual small conductance ion channel, the plasmodial surface anion channel (PSAC). Because these increases may be essential for parasite survival in the bloodstream, an important question is whether other intraerythrocytic parasites induce similar ion channels. Here, we examined this question using human erythrocytes infected with Babesia divergens, a distantly related apicomplexan parasite that can cause severe disease in immunocompromised humans. Osmotic lysis experiments after enrichment of infected erythrocytes with a new method revealed that these parasites also increase host permeability to various organic solutes. These permeability changes differed significantly from those induced by P. falciparum in transport rates, selectivity profiles and temperature dependence. Cell-attached and whole-cell patch-clamp experiments confirmed and extended these Antabuse 200 Mg differences because neither PSAC-like channels nor significant increases in whole-cell anion conductance were seen after B. divergens infection. While both babesia and plasmodia increase host erythrocyte permeability to a diverse collection of organic solutes, they utilize fundamentally different mechanisms.

micronase drug interactions 2015-10-03

Erythrina variegata Linn. (Fabaceae), commonly known as Tiger's Claw, is a thorny deciduous tree grown in tropical and subtropical regions of Eastern Africa, Southern Asia, and Northern Australia. In India, its leaves are Nolvadex Uk Buy traditionally used for diabetes mellitus.

micronase generic name 2017-06-21

We propose that ATP-sensitive K(+) (K(ATP)) channels are normally inactive but involved in beta(2)-adrenoceptor stimulated relaxation of the rat bladder. Spontaneous detrusor muscle contractions were unaffected by glibenclamide (K(ATP) channel blocker) but were reduced when pinacidil (K(ATP) channel opener) Exelon Oral Medication concentrations exceeded 10(-5) M. Inhibition by beta(2)-adrenoceptor agonist clenbuterol [10(-6) M] of 1 Hz electrical field stimulated contractions was abolished by glibenclamide [10(-6) M]. Glibenclamide [10(-6) M] decreased forskolin-induced relaxation [10(-9)-10(-4) M] in bladder muscle stimulated with 1 Hz electrical field. In the presence glibenclamide (10(-6) M) or myristoylated protein kinase A inhibitor (2)x[10(-6) M], clenbuterol [10(-9)-10(-5) M] failed to inhibit bladder contraction in response to 1 Hz electrical field stimulation. Therefore, K(ATP) channel opening and the subsequent hyperpolarization of cell membranes in response to beta(2)-adrenoceptor activation is mediated by raised cyclic-AMP levels and activation of protein kinase A. This counteracts ATP-stimulated depolarization in bladder muscle, thereby reducing cell contraction.

micronase cost 2015-08-27

Isolated aortic rings of rats exhibited relaxant reactivity to Na(2)SO(3)/NaHSO(3) (0-12 mmol/L) in a concentration-dependent manner. IC(50) of the relaxation curve was (7.28+/-0.12) mmol/Lìand Emax Evista Drug Class was 78.79%+/-3.24%. Glibenclamide (1x10(-6) mol/L) inhibited the vasorelaxation to low dose Na(2)SO(3)/NaHSO(3) (6 mmol/L). Nicardipine (1x10(-9) mol/L) could decrease the contraction of the rings to NE, and even could inhibit the relaxation of Na(2)SO(3)/NaHSO(3) almost completely. The inhibition of the endogenous SO(2) production with HDX (1x10(-4) mol/L), resulted in an increase in the contraction of rings. The contraction curve to NE shifted to the left, and IC(50) also changed from (6.48+/-0.84)x10(-7) mol/L to (3.97+/-1.63)x10(-7) mol/L (P<0.01). However, after the incubation of aortic rings with Na(2)SO(3)/NaHSO(3) (4 mmol/L), the contraction curve to NE shifted to the right, and IC(50) changed from (6.48+/-0.84)x10(-7) mol/L to (4.93+/-0.81)x10(-5) mol/L (P<0.01).

micronase drug class 2016-02-19

To investigate the interindividual variation in the absorption of sulphonylureas and its relation to unexpected hypoglycaemia during therapy with these drugs, serum concentration profile of glibenclamide, as well as plasma glucose and insulin response after an oral intake of glibenclamide were studied in 17 patients with non-insulin-dependent diabetes mellitus. In 12 patients glibenclamide was rapidly absorbed, reaching a peak concentration of 138.0 +/- 15.8 ng/ml (mean +/- SEM) at about 2 h. However, in 5 patients the absorption of glibenclamide was delayed and reached a serum peak of 134.1 +/- 29.5 ng/ml at later than 4 h. This delayed absorption was reproducible. There were no significant differences in age, duration of diabetes, per cent of ideal body weight, fasting plasma glucose or HbA1C between the rapid absorption group and Zovirax Acyclovir Review the delayed group. However, autonomic nerve function, assessed by coefficient of variation of R-R intervals, was significantly impaired in the latter group in comparison with the former. Plasma glucose and insulin response to glibenclamide was also delayed in the delayed absorption group.

micronase 10 mg 2015-07-02

Ischemic preconditioning defines an adaptive endogenous mechanism in which a brief episode of reversible ischemia renders the heart more resistant to a subsequent period of sustained ischemia. Because the cardioprotective effects of ischemic preconditioning might be mediated by an activation of adenosine triphosphate-sensitive potassium channels, this study was designed to assess whether these effects could be duplicated by the preischemic administration of a potassium channel opener. Fifty isolated isovolumic buffer-perfused rat hearts underwent 45 minutes of normothermic potassium arrest followed by 1 hour of reperfusion. They were divided into five equal groups that differed with regard to the preconditioning regimen: Group 1 hearts were left untreated and served a controls; in group 2, preconditioning was achieved with 5 minutes of total global ischemia followed by 5 minutes of buffer reperfusion before cardioplegic arrest; in group 3, the preconditioning stimulus consisted of a 5-minute infusion of the potassium channel opener nicorandil (10 mumol/L) followed by 5 minutes of drug-free buffer perfusion before arrest; group 4 hearts underwent a similar protocol except that the infusion of nicorandil was preceded by that of the potassium channel blocker glibenclamide (10 mumol/L); group 5 hearts were ischemically preconditioned like those of group 2 except that the no-flow preconditioning period was also preceded by a 5-minute infusion of glibenclamide (50 mumol/L). The results demonstrate that ischemic preconditioning significantly improved contractility and reduced contracture during reperfusion, as compared with results in control hearts. These protective effects were duplicated by pretreatment with nicorandil but were abolished when the drug was antagonized by a prior infusion of glibenclamide. Likewise, the glibenclamide-induced blockade of potassium channels largely blunted the beneficial effects of ischemic preconditioning. These data suggest that opening of adenosine triphosphate-sensitive potassium channels substantially contributes to preconditioning-induced cardiac protection in a surgically relevant model of global ischemia and, consequently, that the use of potassium channel openers like nicorandil could be an effective means of enhancing cardioplegic protection.

micronase 5 mg 2017-06-15

The effects of the K(+) channel opener, pinacidil on the spontaneous rhythmic contractions and contractions provoked by electrical field stimulation (50 Hz) or by oxytocin were investigated in the isolated uterus of the non-pregnant rat in oestrus. Pinacidil produced more potent inhibition of oxytocin-elicited contractions than of spontaneous rhythmic contractions or electrical field stimulation-induced contractions. Glibenclamide, a selective blocker of adenosine triphosphate (ATP)-sensitive K(+) (K(ATP)) channels, antagonized the pinacidil-induced inhibition of contractions elicited by oxytocin in a competitive manner. However, the pinacidil-induced inhibition of electrical field stimulation-elicited contractions and spontaneous rhythmic contractions was antagonized non-competitively by glibenclamide. In the uterine strips pre-contracted with 80 mM K(+), the pinacidil-induced maximal relaxation was not affected. The present data show that pinacidil exhibits potent relaxant properties in the rat non-pregnant uterus in oestrus and therefore should be taken into account as a possible agent for treatment of dysmenorrhoea. Based on glibenclamide affinity, it appears that the inhibitory response to pinacidil involves K(ATP )channels. We need further investigations to explain why the interaction between glibenclamide and pinacidil in this experimental model depends on the nature of contractions. The ability of pinacidil to completely relax the rat non-pregnant uterus pre-contracted with K(+)-rich solution suggests that K(+) channel-independent mechanism(s) also play a part in its relaxant effect.

micronase dosage 2016-06-29

Excipients are defined as inert substances added to a drug or food to confer a suitable consistency, appearance, or form. They may be added for bulk, to change dissolution or the kinetics of absorption, to improve stability, to influence palatability, or to create a distinctive appearance. The last function may depend heavily on the use of coloring agents, especially when there are multiple dosages (such as with warfarin), and dose confusion may result in profound complications. While described as inert, excipients have been associated with triggering immunological reactions, although this is almost never considered in common practice when patients have reactions to medications, even when they appear to react to many different and distinct drugs. We have found a cohort of 11 patients with chronic, unexplained pruritic skin disorders that have responded to medication changes centered around avoidance of coloring agents, particularly FD&C Blue No. 1 (bright blue) and Blue No. 2 (indigo carmine). We believe that reactions to agents that color medications and foods may be more common than previously appreciated and that recognition of this phenomenon may provide therapeutic alternatives to patients with intractable pruritic disorders.

micronase 50 mg 2016-09-18

Reductions from baseline to week 24 in HbA1c were observed in all saxagliptin treatment groups versus placebo: saxagliptin 2.5 or 5 mg plus metformin (mean difference from placebo, -0.87% and -0.89%, respectively), glyburide (-0.51% and -0.52%), or thiazolidinedione (-0.45% and -0.60%). Improvement was also observed in FPG and PPG-AUC. Adverse events for the US cohort were consistent with previously reported data from the 3 trials. The pooled incidence of reported hypoglycemia was 5.3% and 11.4% with saxagliptin 2.5 and 5 mg/d add-on, respectively, versus 6.8% with placebo add-on.