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Zantac (Ranitidine)

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Generic Zantac is a high-quality medication which is taken in treatment of intestines, ulcers in the stomach, Zollinger-Ellison syndrome, gastroesophageal reflux disease (GERD) and other conditions of heartburn. Generic Zantac acts by decreasing the amount of acid produced in the stomach. It is a heartburn medicine.

Other names for this medication:

Similar Products:
Axid, Pepcid, Tagamet , Pepcid, Fluxid, Pepcid AC


Also known as:  Ranitidine.


Generic Zantac is a perfect remedy in struggle against intestines, ulcers in the stomach, Zollinger-Ellison syndrome, gastroesophageal reflux disease (GERD) and other conditions of heartburn.

Generic Zantac acts by decreasing the amount of acid produced in the stomach. It is a heartburn medicine.

Zantac is also known as Ranitidine, Monorin, Histac, Ranitil.

Generic name of Generic Zantac is Ranitidine.

Brand names of Generic Zantac are Zantac, Zantac 150, Zantac 300, Zantac 300 GELdose, Zantac 75, Zantac EFFERdose, and Zantac GELdose.


Generic Zantac is available in tablets (150 mg, 300 mg), capsules, syrup.

Before swallowing, fizzy tablets of 25 ml should be dissolved in 1 teaspoon of water.

Before drinking Generic Zantac granules should be mixed with 6 to 8 ounces of water.

The treatment can take more than 8 weeks.

Keep Generic Zantac away from children and do not share it with other people.

Take Generic Zantac tablets orally with water.

Do not crush or chew it.

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


If you overdose Generic Zantac and you don't feel good you should visit your doctor or health care provider immediately. Symptoms of Generic Zantac overdosage: coordination, feeling light-headed, fainting.


Store at room temperature between 2 and 30 degrees C (36 and 86 degrees F) away from moisture, light and heat. Keep container tightly closed. Throw away any unused medicine after the expiration date. Keep out of the reach of children.

Side effects

The most common side effects associated with Zantac 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.


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

Be careful with Generic Zantac if you're pregnant or you plan to have a baby, or you are a nursing mother.

Generic Zantac can increase a risk of developing pneumonia.

Be careful using Generic Zantac if you are taking triazolam (Halcion).

It can be dangerous to use Generic Zantac if you suffer from or have a history of kidney disease, liver disease, phenylketonuria (PKU), porphyria.

Avoid alcohol.

Do not stop taking Generic Zantac suddenly.

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In our recent study, oral cimetidine increased carbamazepine plasma levels after a single oral dose by 26 percent and prolonged the elimination half-life by 18 percent. This effect of cimetidine on carbamazepine could have resulted from enhanced carbamazepine absorption and/or inhibited metabolism. To gain an insight into which mechanism was responsible, we repeated the study with ranitidine, which has nearly identical gastrointestinal effects as cimetidine, but does not inhibit oxidative metabolism. Eight healthy subjects received a single dose of carbamazepine 600 mg po on two occasions separated by one month. In a randomized sequence, they also received ranitidine 300 mg/d or matching placebo starting two days before and continuing until seven days after the carbamazepine dose. Ranitidine did not change the carbamazepine area under the plasma concentration-time curve (324.2 +/- 71.1 micrograms h/ml, placebo vs. 326.3 +/- 65.0 micrograms h/ml, ranitidine; p = 0.84) or the elimination half-life (32.2 +/- 6.4 h, placebo vs. 31.7 +/- 6.1 h, ranitidine; p = 0.62). Since ranitidine does not alter the pharmacokinetic profile of oral carbamazepine, it is unlikely that the changes observed with cimetidine were due to increased carbamazepine absorption. Therefore, the mechanism of the single-dose carbamazepine-cimetidine interaction is probably metabolic inhibition, although the exact pathway (or pathways) affected has not been identified.

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The efficacy and safety of famotidine and ranitidine in the treatment of active duodenal ulcer were compared in a multicenter, randomized double-blind study. The study was carried out in 5 centers which included a total of 143 patients with endoscopically documented active duodenal ulcer. The patients received either famotidine (1 tablet of 40 mg at night) or ranitidine (2 tablets of 150 mg at night). Endoscopic examinations were performed at 4 and 6 weeks of active treatment. Day and nocturnal pain were also monitored and the laboratory and clinical profiles evaluated. One hundred and thirty-three patients fulfilled the evaluation criteria (66 patients in the famotidine group and 67 in the ranitidine group). Healing rates at weeks 4 or 6 of treatment showed no significant differences between the famotidine and the ranitidine groups. The healing rates were 79% at week 4 and 96% at week 6 in the famotidine group, and 77% at week 4 and 95% at week 6 in the ranitidine group. Similar results were observed in both treatment groups with regard to pain resolution, decrease in antacid intake and safety profile.

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Ranitidine is a generally well-tolerated drug, and serious side effects are rare. However, ranitidine-induced anaphylaxis has been reported on rare occasions. We report on such a case and review other cases reported in the literature.

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A double-blind clinical investigation was conducted to study the effectiveness of ranitidine therapy in 52 patients with gastritis that had been confirmed by panendoscopy. Subjective weekly assessment of symptoms showed that patients receiving 300 mg of ranitidine daily for four weeks improved considerably more than those receiving placebo. In the ranitidine-treated group, symptoms completely disappeared in 20 (80%) of 25 patients and significantly improved in the other five; in the placebo group, only nine (45%) of 20 patients improved, with the remaining 11 staying unchanged (seven patients--one in the ranitidine-treated group and six in the placebo-treated group--did not return to the hospital and so were withdrawn from the study). Panendoscopy repeated in 41 patients at the end of the four-week treatment period confirmed the assessment of symptoms. No significant adverse effects were observed in patients taking ranitidine. This investigation found ranitidine to be an effective short-term treatment for patients with endoscopically proved gastritis.

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Ranitidine clearance by hemodialysis is significantly higher with PS than with CP. Although additional dose adjustment may not be needed for ranitidine, the type of dialyzer membrane can affect drug elimination and should be taken into account for consideration of drug removal by hemodialysis.

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There is obvious advantage in treating peptic ulcers by the combination of Jianweiyuyang granules and ranitidine capsules, and its mechanisms may be to protect the gastric mucosal barrier by up-regulating the expression of MUCSAC mRNA and to improve the gastric mucosal blood flow by down-regulating the expression of ETAR mRNA.

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1. Twelve healthy men drank 0.80 g ethanol kg-1 body weight on four occasions spread over several weeks. Ethanol was given as 96% v/v solvent which was diluted with orange juice to make a cocktail (20-25% v/v). This drink was ingested in exactly 30 min at 08.00 h after an overnight (10 h) fast. 2. Samples of venous blood were obtained at exactly timed intervals of 0, 10, 20, 30, 45, 60, 90, 120, 150, 180, 240, 300, and 360 min after the start of drinking. The concentrations of ethanol in whole blood were determined by headspace gas chromatography. 3. Summary measures were used to evaluate the concentration-time profiles of ethanol for each subject. The between-subject and within-subject components of variation for the pharmacokinetics of ethanol were derived by one-way analysis of variance (ANOVA). 4. The variation between different subjects dominated the total variance for all of the pharmacokinetic parameters studied except the rate of disappearance of ethanol from blood (ko). For this latter parameter, 42% and 58% of the total variation arose from variations between- and within-subjects respectively. These results might be important to consider when experiments on the clinical pharmacokinetics of ethanol are being planned.

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To study two groups of patients intubated with different prophylaxis of stress gastric ulcer in a prospective randomized trial. The differential effect on gastric pH, gastric colonization and the incidence of pneumonia associated to mechanical ventilation (PMV) were analyzed.

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1. The effects of single daily doses of 20, 50 and 150 mg of WY-45,727, a novel H2-receptor antagonist, and placebo were compared using long term pH-monitoring in 20 male volunteers. 2. Intragastric acidity was measured using combined Ingold glass electrodes. Subjects underwent four studies each under identical dietary conditions. Medication was taken after the evening meal. 3. Median 24 h pH rose from 1.3 (1.2-1.4 interquartile range) on placebo to 1.9 (1.6-2.8) on 20 mg WY-45,727, to 3.1 (2.3-3.7) on 50 mg WY-45,727 and to 4.5 (3.7-4.7) on 150 mg WY-45,727. All three doses increased 24 h and night-time pH significantly compared with placebo (P less than 0.0001). 4. The PAGE test for order effects confirmed clear dose dependent inhibition of acidity (P less than 0.0001). 5. Highly consistent individual responses were found during the night following 150 mg WY-45,727.

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To compare the efficacy of omeprazole, a proton pump inhibitor, with Histamine H2 receptors antagonists in the control and recurrence of non-variceal upper gastrointestinal bleeding.

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Antiulcer activity of Andrographis paniculata was evaluated by cysteamine induced duodenal ulcer model in rats. Male albino Wistar rats were pre-administered with 200 mg/kg body wt. of hydroalcoholic extact of Andrographis paniculata (HAEAP) orally, for 30 days prior to i.p. administration of 420 mg/kg body wt. of cysteamine as a single dose. Rats preadministered with 30 mg/kg body wt. of ranitidine served as standard drug. Ulcer index, thiobarbituric acid reactive substances, mucin, glutathione peroxidase and myeloperoxidase activities, reduced glutathione/oxidized glutathione (GSH/GSSG) ratio, glycoproteins and membrane bound enzyme activities were measured in duodenum of experimental animals. The ulcer score and myeloperoxidase activity were significantly minimized in rats treated with HAEAP. Mucin content was found to be preserved in rats treated with the extract. GSH/GSSG ratio and glutathione peroxidase activities were found to be maintained by the HAEAP. Level of lipid peroxidation products was found to be significantly low in HAEAP treated rats compared to ulcer control rats. The basolateral and brush border membrane bound enzyme activities which were depleted significantly in ulcer control rats were found to be maintained in rats pre-treated with the extract. The ulcer preventing effect was comparable to that of ranitidine treated rats. Level of glycoproteins was also found to be preserved in rats treated with the extract. The normal rats treated with the HAEAP did not show any abnormal alterations in the parameters studied. Histopathological observations also showed the ulcer preventing effect of the HAEAP. It is suggested that the ulcer preventing effect may be due to its mucin preserving and antioxidant nature.

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Transient ischemia was produced for 15 min by occlusion of the middle cerebral artery in halothane-anesthetized rats, and changes in the extracellular concentrations of neurotransmitter monoamines and amino acids were examined in the striatum. The occlusion produced marked increases in the extracellular concentrations of both dopamine and glutamate in the striatum in the saline-injected control group, the peak values being 148 and 5.2 times those before ischemia, respectively. Preischemic administration of histamine (200 nmol, i.c.v.) suppressed the increase in dopamine and glutamate levels during ischemia, the peak values being 38% and 40% of those in the control group, respectively. Neither the dopamine nor glutamate level was affected by 6-[2-(4-imidazolyl)ethylamino]-N-(trifluoromethylphenyl)heptanecarboxamide (HTMT), an H(1) agonist (100 nmol, i.c.v.). However, dimaprit, an H(2) agonist (100 nmol, i.c.v.) suppressed the peak values to 42% and 32%, respectively. Most neurons were degenerated 7 days after ischemia in control animals. Histologic outcome was alleviated by either histamine or dimaprit treatment, whereas HTMT did not affect the outcome. Although postischemic administration of mepyramine, an H(1) antagonist (5 nmol, i.c.v.), did not affect the histologic alleviation caused by preischemic treatment with histamine, ranitidine, an H(2) antagonist (30 nmol, i.c.v.), partly abolished the improvement caused by histamine. These results suggest that suppression of ischemic release of excitatory neurotransmitters by histamine H(2) action is a contributing factor in alleviation of histologic outcome.

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Histopathologically the glucocorticoid group showed wide medullary cavities with wide osteocytic lacunae. These marrow cavities were reduced in the prophylactic groups (III, IV) but increased in group V. Bone histomorphometric analysis revealed improvement in static bone parameters in groups III and IV and deterioration in group V in comparison to group II. The DEXA revealed significant reduction in the bone mineral density in all experimental groups compared to the control group.

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Using a randomized 4-way cross-over design, cats were given enteric-coated omeprazole granules (1.1-1.3 mg/kg q24h and q12h), ranitidine (1.5-2.3 mg/kg q12h), and placebo. Intragastric pH was monitored continuously for 96 hours using the Bravo(™) system, starting on day 4 of treatment, followed by a median washout period of 12 days. Mean percentage of time pH was ≥3 and ≥4 was compared among groups using repeated measures ANOVA.

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H. pylori was cultured and clarithromycin susceptibility was determined before and after treatment, from duodenal ulcer patients receiving RBC and clarithromycin or omeprazole and clarithromycin for 2 weeks in a multicenter randomized clinical trial.

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The focus was on haloperidol (central dopamine antagonist)-stomach lesion, a longly described suitable counterpart of dopamine blocker cysteamine-duodenal lesion. In this, the contribution of blockade of central/peripheral dopamine receptors and prostaglandins synthesis, along with influence of antiulcer agents was evaluated in mice. Male NMRI Hannnover mice were sacrificed 24 h after haloperidol (25 mg/kg b.w. i.p., given alone or with saline (haloperidol+saline) (i) or in combination (ii,iii)). Supporting central dopamine predominance for haloperidol stomach lesion induction, co-administration of peripheral dopamine receptor antagonist domperidone (5 mg/kg i.p.) (haloperidol+ domperidone) (ii), or prostaglandin synthesis inhibitor indomethacin (10 mg/kg s.c.) (haloperidol+ indomethacin) (iii) did not aggravate this lesion. (i) In haloperidol+saline challenged mice the lesions were inhibited by co-administration (/kg i.p.) of a gastric pentadecapeptide BPC 157, GlyGluProProProGlyLysProAlaAspAspAlaGlyLeuVal, M.W. 1419 (10 microg, 10 ng, 10 pg, but not 1 pg, 100 fg, 10 fg), bromocriptine (10 mg), omeprazole (10 mg, 100 mg, but not 1 mg). Atropine (10, 100, 200 mg), pirenzepine (10, 100, 200 mg), misoprostol (10, 100, 200 microg), pantoprazole (1, 10, 100 mg), lansoprazole (0.1, 1, 10 mg), cimetidine (10, 100, 200 mg) and ranitidine (10, 100, 200 mg) were not effective. (ii) Dopamine peripheral blockade influence: in haloperidol+domperidone mice, previously effective bromocriptine, pentadecapeptide BPC 157 (10 microg) or omeprazole (10 mg) did not attenuate stomach lesions. (iii) Prostaglandins synthesis blockade effect: in haloperidol+indomethacin mice, previously effective agents, bromocriptine or omeprazole were not active, while BPC 157 effect was only lessened.

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To verify if cimetidine, ranitidine, and famotidine, when inoculated by ip route in mice, do enhance macrophage activation and whether or not such activation is altered with prior use of sodium thioglycolate. KIND OF STUDY: Experimental.

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The pathophysiology of stress ulcers is complex. There is either too much acid and pepsin or inadequate mucosal defenses. The incidence of upper GI bleeding due to stress ulcers in the ICU is 5-25% depending upon the minimum criterion of bleeding. For the individual patient the risk of bleeding is determined by his underlying condition and the number of risk factors. SAPS and APACHE II may assist in identifying those patients. Attainment of an increase in intragastric pH is effective and frequently necessary to prevent stress ulcer bleeding and reduces the incidence of overt bleeding. Based on presently available information the most suitable regime for prevention of stress ulcer bleeding is a continuous infusion or fixed bolus dosing of cimetidine or ranitidine. With respect to the side effects, ranitidine appears to be the more favorable of these two H2 blockers. The position of sucralfate in the prophylaxis has not yet been established.

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Although gastric acidity is essential for the development of DU, the pathogenesis is more complex and includes an imbalance in the "defending" forces, mainly in mucous secretion, prostaglandin and bicarbonate synthesis and cell turnover. The new drugs available for inhibition of acid secretion, ulcer isolation and cytoprotection make it possible to attack the problem from different sites. The decision of which drug to choose should take into account side effects, drug interactions, cost and recurrence.

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One hundred and twenty patients were randomly divided into 6 groups. Another 10 patients as the control group were confirmed with no peptic ulcers by endoscope, but had digestive tract symptoms. The clinical effects were compared among each group after the one month treatment.

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Intravenous cimetidine, 300 mg or 400 mg, or ranitidine, 50 mg, was administered as a single dose to 36 volunteers in a randomized, crossover fashion. Aspirates of gastric juice were obtained after dosing, and the pH, titratable acidity, gastric fluid volume, and gastric acid output were determined from baseline through 71/2 hours for each subject. Each intervention significantly increased pH and suppressed hydrogen ion concentration, gastric fluid volume, and gastric acid output. Both the magnitudes of the changes when compared with baseline and the time of the mean maximum effects were similar in all three drug regimens. The effect of all three interventions on gastric fluid volume and gastric acid output diminished sharply after 6 hours. The data indicate that the gastric secretory response to all three interventions did not differ substantially.

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PVC matrix membrane selective electrodes for ranitidine, nizatidine and famotidine, based on sparingly soluble complexes, were prepared and characterized. The optimum functional pH range, response time, selectivity and lifetime were determined for each of the built electrodes. The linear range, precision and accuracy of each method were obtained by statistical interpretation of experimental results, while the limit of detection and thelimit of quantification were determined by a graphical method. All these electrodes were applied for the direct quantitative potentiometric determination of ranitidine hydrochloride, nizatidine and famotidine in pharmaceutical formulations.

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No implications for practice at this stage can be concluded. Appropriately designed large-scale randomized controlled trials with long-term follow up are needed to determine the effects of additional bedtime H(2)RAs in suppressing NAB.

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H2R-ANT adjunctive therapy did not improve overall symptoms. To clarify the opposite results between body weight and BMI, future research should investigate long-term efficacy and generate more safety data by using larger samples.

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Problems after Helicobacter pylori (Hp) eradication therapy include recurrence of Hp-negative peptic ulcers. We investigated the pathophysiological characteristics of Hp-negative recurrent ulcer scars, and performed proton pump inhibitor (PPI) maintenance therapy as a new therapy for prevention of recurrence in patients with Hp-negative recurrence after Hp eradication and investigated its usefulness.

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This paper reports the results of a multicenter prospective study of 188 consecutive patients affected by gastric ulcer, verified by endoscopy, in whom the frequency of a mycotic infection of the lesion was evaluated as well as the eventual influence of such pathology on the efficiency of medical treatment, the healing rate, and the healing time. A mycotic infection, defined as penetration of the periulcerous mucosa by the fungi, was found in only 13 patients (6.9%). No significant differences were found in the healing rate and healing time among these patients treated with H2-receptor antagonists and a control group of 43 matched gastric ulcer patients treated in the same period with the same therapy. It would appear from the data that mycotic infections of the gastric ulcer do not modify the efficiency of medical treatment.

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zantac 48 tablets 2015-10-18

Each subject was given a single dose of saquinavir mesylate 600 mg with one of three randomly assigned treatments: ranitidine 150 mg on the evening before and 150 mg on the day of study drug administration, without food (treatment A); ranitidine 150 mg on the evening buy zantac before and 150 mg on the day of study drug administration, with food (treatment B); and with food alone (treatment C, control). After a 7-day washout period between each of the interventions, subjects received the other two treatments.

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Cumulative healing at 12 weeks was 93% on colloidal bismuth subcitrate (of 92 patients) and 97% on ranitidine (of 102 patients). Relapse at 1 year was significantly less on active treatment as follows: placebo (50 patients) 60%; ranitidine (71 patients) 21%; colloidal bismuth subcitrate (64 patients) 33%. This was independent of the results of buy zantac the rapid urease test which was positive in 78%, 88% and 76% of the patients respectively. Treatment was well tolerated. The highest median blood bismuth level (mcg/L) was 25 in the healing phase and fluctuated between 6 and 10 in the maintenance phase.

zantac 500 mg 2016-10-21

All infected patients with a peptic ulcer should be treated for H. pylori. The role of treating H. pylori in patients with undiagnosed dyspepsia or non-ulcer dyspepsia, those taking nonsteroidal anti-inflammatory medications, or with a family history of gastric cancer remains controversial. Triple therapies consisting of a proton pump inhibitor or ranitidine bismuth citrate and two antibiotics are the current standard of therapy for H. pylori. In general, dual therapies should no longer be used to treat H. pylori. Bismuth triple therapy consisting of bismuth, tetracycline, and metronidazole is a less expensive alternative to proton pump inhibitor-or ranitidine bismuth citrate-based triple therapies. However, bismuth triple therapy is hampered by frequent side effects and the need for qid dosing. In Europe, a 7-day course of therapy appears to be adequate. In the United States, 10-14 days of therapy are currently recommended. Metronidazole resistance in H. pylori strains varies geographically, and negatively buy zantac influences the effectiveness of therapies containing this antibiotic. Clarithromycin resistance is relatively infrequent at the current time but may be rising in countries where this antibiotic is in use. If a patient remains infected after a course of therapy for H. pylori, the second treatment should avoid the antibiotics used initially.

zantac kids dosage 2015-02-04

This study tested the hypothesis that chronic exposure to H2-antagonists may affect neuromuscular function. Cimetidine or ranitidine was administered to rats for twenty one days as subcutaneously implanted biodegradable pellets. Control rats received placebo pellets. Serum cimetidine and ranitidine buy zantac concentrations ranged from 0.1 to 0.5 micrograms/mL over this period. On the study day, surgically prepared anaesthetized rats received either succinylcholine (SCh) or atracurium (ATr) to achieve complete paralysis of the tibialis anterior muscle. After recovery an infusion dose of each neuromuscular blocker was titrated to produce 50% muscle paralysis with each blocker. Exposure to cimetidine or ranitidine did not alter SCh or ATr dose to maximum paralysis or the time course of recovery from the initial paralysis. SCh or ATr infusion rates required to elicit 50% paralysis were also unaffected by cimetidine or ranitidine pretreatment. These results indicate that chronic exposure to cimetidine or ranitidine at human therapeutic concentrations does not affect the neuromuscular pharmacodynamics of SCh or ATr in rats.

zantac generic target 2015-10-20

A decision-analytical buy zantac model was developed to estimate expected per patient costs [1998 Canadian dollars ($ Can)], weeks without ulcer and symptomatic ulcer recurrences for the Hp-PAC compared with: proton pump inhibitor (PPI)-clarithromycin-amoxicillin (PPI-CA), PPI-clarithromycin-metronidazole (PPI-CM), PPI-amoxicillin-metronidazole (PPI-AM) and ranitidine-bismuthmetronidazole-tetracycline (RAN-BMT).

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Studies were identified by MEDLINE (January 1982 through December 1997) using the key words H2 receptor antagonists buy zantac and alcohol. Other studies were identified by reviewing bibliographies of retrieved articles and by discussion with colleagues.

zantac 50 mg 2016-02-05

The effects of histamine and related drugs on the evoked tritium overflow from superfused rat brain cortex slices preincubated with 3H-noradrenaline were determined. Tritium overflow was stimulated electrically (3 Hz; slices superfused with normal physiological salt solution) or by introduction of CaCl2 1.3 mmol/l (slices superfused with Ca2(+)-free medium containing K+ 20 mmol/l). Histamine slightly decreased the electrically evoked 3H overflow in slices superfused in the presence of desipramine. The degree of inhibition obtained with histamine was doubled when both desipramine and phentolamine were present in the superfusion medium (pIC15 6.46). Under the latter condition, the evoked overflow was inhibited by the H3 receptor agonist R-(-)-alpha-methylhistamine and its S-(+) enantiomer (pIC15 7.36 and 5.09, respectively), but was not affected by the H2 receptor agonist dimaprit and the H1 receptor agonist 2-thiazolylethylamine (both at up to 32 mumols/l). The concentration-response curve of histamine was shifted to the right by the H3 receptor antagonists thioperamide, impromidine and burimamide (apparent pA2 8.37, 6.86 and 7.05, respectively), by the H2 receptor antagonist ranitidine (apparent pA2 4.27) and was not affected by the H1 receptor antagonist dimetindene (32 mumols/l). The inhibitory effect of R-(-)-alpha-methylhistamine on the evoked overflow was also counteracted by thioperamide. Given alone, none of the five histamine receptor antagonists affected the evoked overflow. In the absence of desipramine plus phentolamine, impromidine and burimamide facilitated the electrically evoked 3H overflow whereas thioperamide had no effect. The facilitatory buy zantac effects of impromidine and burimamide were abolished by phentolamine, but not affected by desipramine.(ABSTRACT TRUNCATED AT 250 WORDS)

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Reports of adverse drug reactions due to histamine H2-receptor antagonists (H2RAs) are rare considering their wide usage. Cimetidine produces central nervous system and endocrine toxicities more often than other H2RAs. Drug-drug interactions are of potentially greater concern with H2RAs, especially because the critically ill patient routinely receives many drugs. H2RAs may alter the absorption, metabolism, or renal excretion of concurrently administered drugs. Gastrointestinal absorption of drugs, such as ketoconazole, that dissolve poorly in the absence of adequate acid may be reduced. Inhibition of hepatic oxidative drug metabolism of agents such as warfarin, theophylline, and phenytoin, is primarily a problem with cimetidine. Adverse effects will be seen in predisposed individuals and the time course will depend buy zantac on the pharmacokinetics of the object drug. The other H2RAs are less likely to inhibit drug metabolism and affect renal clearance of procainamide than is cimetidine.

zantac dosage pediatric 2015-02-01

A method of grading of skin testing was developed using injection histamine as a positive control. This was evaluated by using it on 517 subjects who had severe (WHO category III) exposure to rabies. A premedication protocol consisting of injections pheniramine buy zantac , ranitidine, hydrocortisone and adrenaline was evaluated by using it on fifty one subjects who were skin test positive/hypersensitive to ERIG.

zantac dosage infant 2015-05-19

The influence of ranitidine and cysteamine on intestinal metaplasia was examined in 7-month-old male Crj: CD (SD) rats. At the age of 5 weeks, the animals were treated with 10 Gy doses of X-rays at 3-day intervals up to a total of 20 Gy in the gastric region, and 6 months after irradiation, the rats received either ranitidine (0.02% in diet) or cysteamine (0.1% in drinking water) for 2 months. The incidence and number of intestinal metaplasia with alkaline phosphatase-positive foci in rats given X-rays and cysteamine (group 4) were significantly low compared with those in rats given X-rays and ranitidine (group 3) (p less than 0.01). In both the pyloric and the fundic gland mucosae, the average numbers of type C metaplasia (intestinal crypts with Paneth cells) and total numbers of buy zantac metaplastic foci in rats of group 3 were much higher than those in group 4 (P less than 0.05). The present results showed that the occurrence of intestinal metaplasia was significantly increased after administration of ranitidine and decreased by cysteamine.

zantac tablets 2017-03-27

We report on the case of a 65-year-old female who was treated for one week with famotidine, a reversible H(2)-histamine antagonist, due to gastric pain. Shortly after treatment began, she presented manic symptoms and developed two generalized seizures, after which famotidine was discontinued. Manic symptoms were present for three months; intermittent treatment with both carbamazepine and antipsychotic medication was necessary before her mental status was completely restored. While cimetidine and ranitidine are known to cause secondary mania, this symptom has not been described for famotidine. CNS side effects are usually short-lived and respond to discontinuation of the drug, which was not the case in our patient. During a follow-up period that has so far lasted four years, the patient has been buy zantac stable without any psychiatric medication. Adjusting the maintenance dosage of H(2)-histamine antagonists has been recommended in elderly patients since age-related reduction in renal plasma flow, glomerular filtration rate and renal tubular function may be present, which can in turn elevate histamine levels in plasma and cerebrospinal fluid. Our patient, however, had normal renal function and was free of organic or psychiatric diseases, so what pathogenetic mechanism led to the remarkably long standing manic syndrome after a relatively short course of famotidine remained unknown; famotidine seems to cause the same spectrum of adverse central nervous system (CNS) reactions as other H(2)-histamine antagonists.

zantac generic 2016-08-07

Over the past 20 years, drug use review (DUR) activities have become an integral component of inpatient care to assure that medications are being used in the most cost-effective manner. The term drug use evaluation (DUE) has supplanted DUR, because DUE implies an expansive, integrated program that includes retrospective, concurrent, and prospective drug performance evaluations made possible through automation. DUE monitors drug experience outcomes, which allows the Pharmacy & Therapeutics (P&T) Committee to revise the drug formulary in response to patient care and cost-analysis research. Computerized HMOs are now embracing DUE as a result of the competitive drive to balance quality of care and cost-containment. United HealthCare (UHC) has used DUE to evaluate the cost-effectiveness of therapeutically similar medications. The UHC database captures medical and pharmacy claims data, and allows analysis of the total cost of care. UHC has used the buy zantac system to make rational formulary decisions based on global costs, rather than drug ingredient costs. As data processing systems such as this flourish, other HMOs will be able to conduct similar DUE activities. The HMO environment provides a fertile site for such research to be conducted by pharmaceutical manufacturers.

zantac 75 dosage 2015-02-10

The literature on H2-antagonist drug interactions is now extensive. The whole subject is so complicated as to make things difficult for the potential prescriber. However, it is possible to reduce most of the information contained in the literature to a few simple messages. Firstly, H2-antagonists bind to cytochrome P450 and may inhibit the metabolism of drugs eliminated by the mixed function oxygenase system. In this respect, cimetidine has a marked effect which, in most studies, has reached statistical significance. Ranitidine, on the other hand, has a much weaker effect which, even if demonstrable, is statistically non-significant. The potential benefit of ranitidine, however, has to be weighed against the relative costs of the 2 drugs. Secondly, H2-antagonists inhibit gastric acid production and may alter the rate of gastric emptying, and hence the rate of drug absorption. They may also have some effect on portal vein and hepatic artery flow. However, these effects are small and probably not clinically relevant. Thirdly, pharmacodynamic effects of H2-antagonist-drug interactions are difficult to demonstrate in planned studies, and although they are reported from time to time, adverse reactions of consequence are relatively uncommon. Fourthly, the prescriber needs to be aware that cimetidine may produce higher plasma concentrations of some drugs which have a fairly narrow therapeutic range, and this may be clinically important. Examples of drugs for which it may be undesirable to inadvertently increase plasma concentrations include warfarin Mysoline And Alcohol , theophylline and phenytoin. Finally, for most drugs metabolised by the liver, the risk of an important interaction is small. However, if such an interaction is noted it may be helpful to refer to the other reported cases, and a number of references are included here.

zantac 75 generic 2016-04-01

Of the two major subfractions of high density lipoprotein (HDL), HDL2 cholesterol (HDL2-C) and not HDL3 cholesterol (HDL3-C) correlates negatively with coronary heart disease. To study the effect of cimetidine and ranitidine on HDL subfractions, 6 healthy males received cimetidine (600 mg bid) ranitidine (150 mg bid) and placebo (one tab bid) for 1 week each, in random order. Measurements of HDL cholesterol (HDL-C), HDL2-C, HDL3-C were made on day 7 of each week. Comparing cimetidine with placebo, HDL2-C/HDL-C, HDL2-C/total cholesterol and HDL2-C/HDL3-C increased significantly while HDL3-C/HDL-C decreased. There was no difference in HDL-C parameters between ranitidine and Lopid 300 Mg placebo. Cimetidine treatment results in redistribution of HDL subfractions in favour of HDL2. The mechanism is not H2-receptor antagonism as ranitidine had no such effect.

generic zantac cost 2017-10-09

Initial eradication of H. pylori is the treatment of choice in patients Stromectol Tab 3mg with duodenal ulcer.

zantac 6 tablets 2015-10-07

Four different H2-antagonists caused an increase in the TEER across the Caco-2 cell monolayers, accompanied by a decrease in the permeability for mannitol. The effect was concentration-dependent and saturable. Ranitidine and famotidine, caused a decrease in their own transport rate across the Caco-2 cells. Ranitidine competitively inhibited the increase in TEER caused by famotidine, whereas compounds which represent molecular fragments of ranitidine had no effect. The relative potency of the four H2-antagonists in causing an increase in the TEER correlated inversely with the oral bioavailability of Oxytrol Drug Class these compounds in humans.

zantac dosing information 2016-09-08

To determine whether ranitidine bismuth citrate (RBC) based regimens may be used as second-line treatments after 'Maastricht therapy' Ponstel 250mg Capsules failure.

child zantac dosage 2016-04-27

A bioequivalence study of two oral formulations of 300 mg ranitidine was carried out in 16 healthy volunteers (8 men and 8 women), and the pharmacokinetics in both sexes were compared. There was bioequivalence of both formulations. The terminal half-life of ranitidine was 7% shorter and the oral apparent clearance 10.5% higher in women (1.44 L/h/kg) than in men (1.29 L/h/kg), although this difference did not reach statistical significance. No differences were observed in maximum concentration (Cmax) or the time of its occurrence (tmax). Sex, age, and weight did not correlate significantly with oral clearance. These results suggest that there are no sex differences in the pharmacokinetics of ranitidine, or that any differences would not be of clinical relevance. It also should be emphasized that bioequivalence trials Augmentin 500mg Tab also can be used to study other pharmacokinetic or pharmacodynamic characteristics of drugs without damaging the main endpoint of the study.

zantac 40 mg 2015-11-24

To determine whether a triple therapy regimen for the treatment of Helicobacter pylori infection, consisting of ranitidine 300 mg q.i.d., clarithromycin 500 mg t.i.d., and metronidazole 500 mg t.i.d. would provide a safe and effective treatment regimen, we performed an open prospective study in 20 Zantac Generic Name consecutive patients with proven H. pylori-associated non-ulcer dyspepsia or peptic ulcer disease.

zantac dosing instructions 2015-10-29

To assess the cost effectiveness of a multidrug prepackaged regimen for Helicobacter pylori, the Hp-PAC (lansoprazole 30mg, clarithromycin 500 mg, amoxicillin 1 g, all twice daily), relative to alternative pharmacological strategies in the management of confirmed duodenal ulcer over a 1-year period from 2 Prednisone 5 Mg perspectives: (i) a strict healthcare payer perspective (Ontario Ministry of Health) excluding the patient copayment; and (ii) a healthcare payer perspective including the patient copayment.

zantac dosage instructions 2015-12-23

122 patients with duodenal ulcus have been treated with a cimetidine's single night dose of 800 mg over 6 or 12 weeks. After this period of time, 18 patients still had their wounds without complete healing. This group of patients had been afterwards treated with a combination of ranitidine and sulfacrate over a six weeks period. Only 3 of them achieved a complete ulcus reepitelization, although all of them were clinically asymptomatic. These 3 patients moved to a nightly maintenance treatment guideline of 150 mg of Adalat Reviews ranitidine, but they quickly presented relapses. A significantly higher consumption of tobacco and alcohol was observed among the patients who did not heal after 12 weeks of treatment with cimetidine. On the other hand the rest of the general facts and ulcus endoscopic characteristics have been similar both in patients resistant to cimetidine and in those who had a favorable evolution.

zantac medication 2017-01-24

The results of studies on the effect of cimetidine and ranitidine on the bronchial reactivity in a group of 10 patients with atopic bronchial asthma are discussed. The patients received 800 mg of cimetidine daily for 6 days and, after a three-day interval, 300 mg of ranitidine daily for a further 6 days. Bronchial reactivity was determined with the histamine test, according Requip Pill Identifier to Spector and Farr, before the administration of each drug and on the third and sixth days of each course of the treatment. A comparison of the effect of cimetidine and ranitidine on the bronchial reactivity in the same patients revealed that a 3-day exposure to each of the two drugs, cimetidine enhanced bronchial reactivity to a greater extent than ranitidine; the difference between the action of the two drugs being statistically significant (p less than 0.05). Bronchial reactivity was found to increase significantly after a 6-day treatment with each of the drugs but no statistically significant differences were noted comparing the effect of these drugs.