Generic Imdur is an effective medication which helps in the treatment of angina attacks. Generic Imdur acts as nitrates.
Other names for this medication:
Also known as: Isosorbide Mononitrate.
Generic Imdur is a perfect remedy, which helps to treat angina attacks.
Generic Imdur acts as nitrates.
Imdur is also known as Isosorbide Mononitrate.
Generic name of Generic Imdur is Isosorbide Mononitrate.
Brand names of Generic Imdur are Imdur, ISMO, Monoket.
Take Generic Imdur tablets orally with or without food.
Do not crush or chew it.
Take Generic Imdur at the same time with water.
If you want to achieve most effective results do not stop taking Generic Imdur suddenly.
If you overdose Generic Imdur and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Imdur are difficult or slow breathing, muscle cramps, nausea, vomiting, diarrhea, high temperature, fainting, abnormal heartbeat, changes in vision, flushing, convulsions, severe throbbing migraine, lightheadedness.
Store at room temperature between 15 and 30 degrees C (59 and 86 degrees F) away from moisture and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.
The most common side effects associated with Imdur are:
Side effect occurrence does not only depend on medication you are taking, but also on your overall health and other factors.
Do not take Generic Imdur if you are allergic to Generic Imdur components.
Do not take Generic Imdur if you're pregnant or you plan to have a baby.
Do not use potassium supplements or salt substitutes.
Be careful using Generic Imdur if you take dihydroergotamine (D.H.E. 45); or any other heart medicines, especially those used to treat high blood pressure or irregular heartbeats.
Be careful using Generic Imdur if you suffer from or have a history of congestive heart failure, have low blood pressure; a stroke, a transient ischemic attack (TIA, or mini-stroke), have anemia; have an allergy to nitrates; have closed-angle glaucoma; migraines, kidney disease; liver disease, heart attack, a serious head injury.
If you want to achieve most effective results without any side effects it is better to avoid alcohol.
Be very careful when you are driving machine.
Do not stop taking Generic Imdur suddenly.
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In 10 healthy male subjects the pharmacokinetics and haemodynamic effects of sustained-release isosorbide-5-mononitrate 60 mg (IS-5-MN) were studied after oral administration at two different times in the day (08.00 h and 20.00 h). Effects on blood pressure and heart rate after 3 min standing upright were measured in relation to the individual circadian control values. The pharmacokinetic parameters (Cmax, tmax, AUC, t 1/2) did not differ after morning and after evening dosing, tmax being 5.2 h and 4.9 h, respectively. In contrast, the cardiovascular effects of IS-5-MN were clearly circadian phase-dependent. The maximum decrease in blood pressure decrease and increase in heart rate occurred significantly earlier after the evening (BPsys 2.8 h; BPdia 2.9 h; HR 3.8 h) than after the morning dose (BPsys 5.0 h; BPdia 6.0 h; HR 5.2 h). Thus, the peak haemodynamic effects coincided with the peak drug concentration after the morning dose, whereas the peak effect was in advance of the peak drug concentration after the evening dose of IS-5-MN. The data provide evidence of circadian phase-dependency in the dose-response relationship of oral IS-5-MN.
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This study was designed to determine the extent, to which isosorbide-5-mononitrate (5-ISMN) contributes to the hemodynamic effect of isosorbide dinitrate (ISDN) in conscious dogs. Test drugs (ISDN or 5-ISMN) were given orally. Either ISDN or 5-ISMN produced a decrease in blood pressure dose-dependently, the decrease in pulse pressure being specific; the pattern of blood pressure change induced by ISDN or 5-ISMN was different from that induced by nifedipine or prazosin. The effect of ISDN (2 mg/kg) was almost equivalent to that of 5-ISMN (4 mg/kg) and the effect of ISDN (4 mg/kg) to that of 5-ISMN (8 mg/kg). After administration of ISDN, both ISDN and 5-ISMN appeared in the plasma, and the effect of ISDN well-correlated with the increase in the plasma concentration of 5-ISMN. Contribution of 5-ISMN to the effect of ISDN was estimated to be about 30% from the value of the plasma concentration of 5-ISMN at 3 to 4 hr after administration, when the maximal response to ISDN occurred. Based on the data of the area under the plasma concentration curve of 5-ISMN (from 0 to 10 hr after administration), the fraction of biotransformation to 5-ISMN from ISDN was calculated to be 73.6 to 76.6% (based on moles). Because the ability of 5-ISMN to decrease pulse pressure was about 1/2 (or 41% based on moles) of that of ISDN, the contribution of 5-ISMN to the effect of ISDN was estimated to be about 30% in total, the value being similar with that estimated at 3 to 4 hr after administration.
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To investigate the effect of different nitrates on isolated rabbit hearts and aortic strips and the mechanism responsible for nitrate tolerance, using nitroglycerine (NTG), isosorbide dinitrate (ISDN), 5-mononitrate (5MN) and 2-mononitrate (2MN).
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One hundred and forty-four MHD patients with hypertension were enrolled in this perspective, randomized, controlled, single-center trial. All patients accepted antihypertensive drugs at baseline, including renin-angiotensin system inhibitor, calcium channel blocker, ß-receptor blocker or a-receptor blocker. Seventy-two patients (nitrate group) took isosorbide mononitrate 30 mg daily, titered to a maximal dosage of 120 mg daily for 24 weeks. The dosage was adjusted once a week according to BP. The remaining 72 patients (non-nitrate group) did not take nitrate drugs other than antihypertensive drugs. BP, left ventricular mass index (LVMI), heart rate, interdialytic weight gain (IDWG) and hemoglobin (Hb) were monitored.
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Nicorandil, an adenosine triphosphate-sensitive potassium channel opener, improves left ventricular (LV) remodeling after myocardial infarction in rat models. However, the effects of chronic nicorandil therapy on cardiac sympathetic nerve activity in patients with ischemic cardiomyopathy have not been determined.
The aim of this work was to optimize time-dependent tablets using artificial neural network (ANN). The time-dependent tablet consisted of a tablet core, which contained sustained release pellets (70% isosorbide-5-mononitrate [5-ISMN]), immediate release granules (30% 5-ISMN), superdisintegrating agent (sodium carboxymethylstarch, CMS-Na), and other excipients, surrounded by a coating layer composed of a water-insoluble ethylcellulose and a water-soluble channeling agent. The chosen independent variables, i.e., X(1) coating level of tablets, X(2) coating level of pellets, and X(3) CMS-Na level, were optimized with a three-factor, three-level Box-Behnken design. Data were analyzed for modeling and optimizing the release profile using ANN. Response surface plots were used to relate the dependent and the independent variables. The optimized values for the factors X(1)-X(3) were 4.1, 14.1, and 29.8%, respectively. Optimized formulations were prepared according to the factor combinations dictated by ANN. In each case, the observed drug release data of the optimized formulations were close to the predicted release pattern. An in vitro model for predicting the effect of food on release behavior of optimized products was used in this study. It was concluded that neural network technique could be particularly suitable in the pharmaceutical technology of time-dependent dosage forms where systems were complex and nonlinear relationships often existed between the independent and the dependent variables.
A case-control study was conducted using the Dutch PHARMO Record Linkage System (1991-2002, n = 6,763 hip fracture cases and 26,341 controls). Cases had their first admission for hip fracture, whereas controls had not sustained any fracture after enrollment. Current users of organic nitrates were patients who had received a prescription within 90 d before the index date. The analyses were adjusted for disease and drug history.
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The hypothesis that nitrates evoke prostacyclin production by vascular endothelium has been reevaluated on cultured umbilical vein endothelial cells and in vascular fragments, both obtained from humans. Endothelial cell monolayers (passages 1 and 2) were washed free of culture medium and exposed for 3 to 5 min to buffer or nitroglycerin (NTG), isosorbide dinitrate (ISDN), or isosorbide-5-mononitrate (ISMN) over a range of concentrations (10(-9)M to 10(-6)M) encompassing those usually attained in vivo, with or without 25 microM sodium arachidonate. Basal prostacyclin production, measured by radioimmunoassay of the stable metabolite 6-keto-PGF1 alpha, depended on cell density in the endothelial monolayer (being higher in preconfluent cultures) and on incubation time. Basal prostacyclin, however, was not altered by incubation with NTG (3.3 +/- 2.0 pg/1000 cells without drug vs 3.9 +/- 3.8 pg/1000 cells with drug, mean +/- SD), ISDN (3.1 +/- 1.9 vs 3.1 +/- 2.2), or ISMN (2.0 +/- 0.9 vs 2.3 +/- 1.5) at 10(-7)M (all differences NS). Also, long-term incubation (2, 6, and 24 hr) with ISDN and ISMN did not alter prostacyclin production over control. Over a 30-fold increase (p less than .001) in prostacyclin production was obtained with arachidonate stimulation, but incubation with nitrates did not significantly modify the stimulated production. Saphenous vein, mesenteric artery, and atrial appendage fragments incubated at 37 degrees C for 20 min in a shaking water bath with a control buffer produced 27.8 +/- 13.9, 189.7 +/- 75.2, and 662.3 +/- 390.6 pg 6-keto-PGF1 alpha/mg tissue, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)
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High plasma levels of isosorbide-5-mononitrate were found in a young girl who had ingested 1.6 g of the drug plus 20 mg of nitroglycerin. These concentrations produced no disturbance of the patient's state of consciousness and no serious haemodynamic effects appeared except for a tachycardia in relation to peripheral vasodilatation.
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The pharmacokinetics of different formulations of glyceryl trinitrate, isosorbide dinitrate, isosorbide 5-mononitrate and isosorbide 2-mononitrate are reviewed.
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The FMD decreased significantly (from 5.97±2.88 to 5.33±2.56%) in the ISMN group, whereas it increased from 6.27±3.23 to 6.96±2.84% in the control group after treatment for 1 year. There was a significant difference in the changes in FMD when the two groups were compared (-0.64±1.83 vs. 0.69±1.77%, P=0.006). There were no significant changes in serum superoxide dismutase, malondialdehyde, and hypersensitive C-reactive protein levels in the two groups.
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Data from this protocol will be used to develop a randomized, controlled trial of nitrates to prevent osteoporotic fractures.
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The aim of this study was to study the hemodynamic effects of orally administered captopril and isosorbide mononitrate in suspected acute myocardial infarction.
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To assess the adverse effects of isosorbide mononitrate (IMN) compared with misoprostol for cervical ripening at term.
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The MTACs of low molecular weight (LMW) solutes in the ISMN period were greater than the placebo period: median urea, 16.7 vs 13.8 ml/min; creatinine (Cr), 7.9 vs 6.9 ml/min; and urate, 6.1 vs 5.5 ml/min (p < 0.05 for all except MTAC of urea). Administration of ISMN could also enhance the clearances of high molecular weight (HMW) solute with a magnitude of increase as follows: 10% for beta2-microglobulin, 50% for albumin, and 15% for immunoglobulin G (p < 0.05 for all). However, the values of restrictive coefficient of LMW as well as HMW solutes of both groups were not different, indicating that the increased solute transports are not due to alteration in the peritoneal membrane permeability. Despite the increased peritoneal solute clearance, net ultrafiltration (UF) was unchanged after drug administration, 110 (ISMN group) vs 120 ml (placebo group), (NS).
Temporary proteinuria occurring after exercise is a common finding, and it is explained predominantly by alterations in renal hemodynamics. In this study, we investigated whether nitric oxide (NO), which is known to have an effect on renal hemodynamics and to increase during exercise, has a role in postexercise proteinuria. In the first step of this study, the effect of acute NO synthase blockage on exercise proteinuria was evaluated. The urinary protein levels in animals that performed acute exhaustive treadmill running exercise were considerably elevated compared with the control animals. Significantly elevated urinary protein levels were also detected in animals that received Nomega-nitro-L-arginine methyl ester before exhaustion, compared with both control and exhausted groups, and mixed-type proteinuria was detected in electrophoresis, as in all exhausted animals. In the second step of the study, a NO donor (isosorbide mononitrate) was given to rats 1 h before exhaustive exercise. Mixed-type proteinuria and the elevation in urinary protein levels that occur as a consequence of exhaustive exercise were prevented by NO donor treatment. Finally, in the third step of our study, a calcium channel blocker (diltiazem), another vasodilator, was applied to the rats 1 h before exhaustive exercise. Urinary protein levels were not different in exhausted rats with or without calcium channel blocker treatment. On the other hand, in both groups, urinary protein levels were higher than in the control group. The tail-cuff blood pressure alterations caused by vasodilator drug applications before exercise were not different for NO donor and calcium channel blocker groups. These results suggest that endogenous NO might prevent the postexercise proteinuria from becoming more severe by affecting hemodynamic changes that occur during exercise.
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This work has been carried out to evaluate over a short and medium space of time (100 days) the efficacy, tolerance and haemodynamic repercussion of 50 mg of sustained release Isosorbide 5-Mononitrate administered once day to patients with stable effort angina in a random and prospective study, which was double blind crossover and placebo-controlled. In this study we included 10 patients who showed positive exercise test using clinical (angina) and electrocardiographic (ischemic drop of the ST greater than 1 mm) criteria. The assessment was done with cycloergometry starting with 30W and increasing by 20W every 2 minutes until angina appeared accompanied by an ischemic drop of the ST. The effort tests were done basally and at intervals of 4, 12 and 24 hours after the dose. The parameters studied were obtained on the 1st, 25th and 100th days of the study and were compared with those of the placebo. The time taken for the ST to 1 mm to fall (seconds) increased when evaluated after 4 and 12 hours on the 1st, 25th and 100th days in comparison with placebo (p < 0.05). The time taken for angina (seconds) to appear lengthened considerably when evaluated 4 and 12 hours after the dose not only on the 1st day but also on the 25th and 100th days in comparison with placebo (p < 0.05). The duration of the effort (seconds) was significantly greater after 4 and 12 hours on the 1st, 25th and 100th days when compared to that of the placebo (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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In a group of 13 patients with severe heart failure, both forced vital capacity (FVC) and forced expiratory volume in 1 s (FEV1) significantly improved after intensive medical therapy (FVC: from 77 +/- 17 to 92 +/- 20%, p < 0.001; FEV1: from 65 +/- 15 to 81 +/- 15%, p < 0.001) in the absence of change in M-mode echo cardiac dimension and left ventricular systolic function; on the other hand, a change of indices of left ventricular filling by Doppler transmitral flow was documented (E/A ratio: from 3.6 +/- 1.2 to 1.65 +/- 1.5, p < 0.01; early filling deceleration time: from 94 +/- 39 to 178 +/- 78 ms, p < 0.01), indicating a reduction of pulmonary capillary pressure; this probably positively affected pulmonary interstitial edema and bronchial wall congestion, thus enhancing pulmonary function.
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Systematic review with meta-analyses of randomized trials on IsMn alone or with beta-blockers or endoscopic therapy for oesophageal varices. Electronic and manual searches were combined. Randomized trials on primary and secondary prevention were included. The primary outcome measure was mortality. Intention-to-treat random effects meta-analyses were performed. The robustness of the results was assessed in trial sequential analyses.
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Differential scanning calorimetry (DSC) is a method which has been applied to obtain thermal information about both raw material and the determination of the content of 5-ISMN in dry mixtures with lactose. The main advantage this offers, compared to other methods, is that it is not necessary to use a standard, it only being necessary to know the data of its fusion heat. HPLC and TLC-densitometry are considered for the determination of 5-ISMN: lactose and pharmaceutical dosage forms. Linearity test, repeatability and accuracy were satisfactory in both methods. Recovery data in pharmaceutical formulations (expressed as the percentage of the label claim) from HPLC and TLC did not give any significant difference (P = 95%). The results show that the chromatographic methods are simple, fast and reliable procedures for the determination of 5-ISMN.
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This review contains recent data on the pharmacokinetics and the hemodynamic effects on heart rate and blood pressure of three different groups of drugs (beta-blockers: propranolol; oral nitrates: isosorbide-dinitrate (ISDN), isosorbide-5-mononitrate (IS-5-MN); calcium channel blockers: nifedipine) which were investigated in healthy volunteers or in hypertensive patients after drug application at different times of the day. In the case of IS-5-MN and nifedipine two different galenic formulations were studied. The results clearly demonstrate chronopharmacokinetics for propranolol, ISDN, and the immediate-release formulations of IS-5-MN and nifedipine, whereas no pharmacokinetic daily variations were observed with the sustained-release formulations. However, all drugs exhibited daily variations in their hemodynamic effects. These data greatly support the view that pharmacokinetics and drug effects should be studied simultaneously when chronopharmacologic studies are performed.
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Outpatient cervical ripening and labor induction with isosorbide mononitrate seems to be an effective, safe, and well tolerated procedure. The definitive clinical efficacy and safety needs to be evaluated in larger series of patients.
Both EVL and drug therapy are effective in the prevention of variceal rebleeding. Comparisons between the two modalities are few, and only in cirrhotics. This prospective randomized controlled trial compared EVL with drug therapy (propranolol + ISMN) in the prevention of rebleeds from esophageal varices in cirrhotic and noncirrhotic portal hypertension (NCPH) patients. One hundred thirty-seven variceal bleeders were randomized to EVL (Group I; n = 71) or drug therapy (Group II; n = 66). In Group I, EVL was done every 2 weeks till obliteration of varices. In Group II, propranolol (dose sufficient to reduce heart rate to 55 bpm/maximum tolerated dose) and ISMN (incremental dose up to 20 mg BD) were administered. Group I and II patients had comparable baseline characteristics, follow-up (12.4 vs. 11.1 months), cirrhotics and noncirrhotics [50(70.4%) and 21(29.6%) vs. 51(77.3%) and 15(22.7%)] and frequency of Child's A (35 vs. 27), B (26 vs. 28), and C (9 vs. 11). The mean daily dose was 109 +/- 46 mg propranolol and 34 +/- 11 mg ISMN and was comparable in cirrhotic and NCPH patients. Upper GI bleeds occurred in 10 patients in Group I (5 from esophageal varices) and in 18 patients in Group II (15 from esophageal varices) (P = 0.06). The actuarial probability of rebleeding from esophageal varices at 24 months was 22% in Group I and 37% in Group II (P = 0.02). The probability of bleed was significantly higher in Child's C compared to Child's A/B cirrhotics (P = 0.02). On subgroup analysis, in NCPH patients, the actuarial probability of bleed at 24 months was significantly lower in Group I compared to Group II (25% vs 37%; P = 0.01). In cirrhotics, there was no difference in the probability of rebleeding between patients in Group I and those in Group II (P = 0.74). In Group II, 25.7% patients had adverse effects of drug therapy and 9% patients had to stop propranolol due to serious adverse effects, none required stopping ISMN. There were 10 deaths, 6 in Group I (bleed related, 1) and 4 in Group II (bleed related, 1); the actuarial probability of survival was comparable (P = 0.39). EVL and combination therapy are equally effective in the prevention of variceal rebleeding in cirrhotic patients. EVL is more effective than drug therapy in the prevention of rebleeds in patients with NCPH and, hence, recommended. However, in view of the small number of NCPH patients, further studies are needed before this can be stated conclusively.
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Irbesartan appears to be the most effective treatment for the combined suppression of blood pressure and AIX in patients with intracranial aneurysms and has a high degree of patient tolerance.
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The objective of this study was to compare NO-donor isosorbide mononitrate to misoprostol, both applied as vaginal tablets for cervical ripening prior to first trimester curettage in patients with missed abortion.
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Extended release formulations of isosorbide mononitrate (IMN), based on osmotic technology, were developed. Target release profile was selected and different variables were optimized to achieve the same. Formulation variables like type (PVP, PEG-4000, and HPMC) and level of pore former (0-55%, w/w of polymer), percent weight gain were found to affect the drug release from the developed formulations. Drug release was inversely proportional to the membrane weight but directly related to the initial level of pore former in the membrane. Burst strength of the exhausted shells was inversely proportional to the level of pore former, but directly affected by the membrane weight. Satisfactory burst strength (more than 320 g) was obtained when PVP was used as pore former (up to 55%, w/w of polymer) at the membrane weight of 7.5% and more. The release from the developed formulations was independent of pH and agitational intensity, but dependent on the osmotic pressure of the release media. Results of SEM studies showed the formation of pores in the membrane from where the drug release occurred. The formulations were found to be stable after 3 months of accelerated stability studies. Prediction of steady-state levels showed the plasma concentrations of IMN to be within the desired range.
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Vaginal application of isosorbidemononitrate in cervical priming prior to curettage abortion is as effective as vaginal application of misoprostol.
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Twenty-six patients with coronary artery disease who had fixed segmental defects on exercise-rest-Tl-201 imaging were studied. All of them underwent Tl-201 reinjection study. Within 1 week of Tl-201 imaging, rest-Tc99m MIBI imaging was performed after sublingual 5 mg ISDN administration (2-day protocol). For each study, tomograms were divided into 20 segments based on three short-axis slices, one vertical long-axis representing the totality of the left ventricle and regional tracer uptake was quantitatively analyzed. Regional tracer uptake was evaluated in 20 myocardial segments for all patients. Viability was defined as presence of tracer uptake >/=50% of peak activity on each study. A total 520 myocardial segments were assessed by semi quantitative analysis.
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Nitrate administration can be safely discontinued in angina-free and hemodynamically stable coronary patients who receive this medication on a regular basis. If relapse of anginal symptoms occurs, it will be within 1 month following nitrate withdrawal, and will resolve satisfactorily with reinstatement of treatment.
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