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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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This study determined the total preparation time, cost, and contamination rate associated with preparing 50-mL admixtures of ranitidine 50 mg from each of the following commercial source vials: 50 mg/2 mL unit-dose vial (treatment A), 50 mg/2 mL 10 mL multidose vial (treatment B), and 50 mg/2 mL 40 mL multidose vial (treatment C). The study consisted of two separate phases: phase I extemporaneous compounding and phase II batch manufacturing. Twelve technicians prepared ten admixtures from each source vial during each phase. All admixtures were tested for sterility; bacterial contamination was not observed. Multidose vials saved approximately $197 per 200 admixtures. Drug and personnel costs were reduced when batch manufacturing with 40-mL multidose vials was compared with extemporaneous compounding with unit-dose vials. Our study showed that multidose vials decreased the total preparation time and cost for making ranitidine admixtures during both extemporaneous compounding and batch manufacturing by reducing setup time, preparation time, and drug procurement cost.

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The compatibility and stability of labetalol hydrochloride in combination with various critical care drugs was evaluated. Labetalol hydrochloride 1.0 mg/mL was combined in 5% dextrose injection with equal volumes of each of the following drugs: dobutamine 2.5 mg/mL (as the hydrochloride salt), dopamine hydrochloride 1.6 mg/mL, morphine sulfate 0.5 mg/mL, nitroglycerin 0.2 mg/mL, and ranitidine 0.6 mg/mL (as the hydrochloride salt). The mixtures were placed in duplicate Y-site administration sets. Visual inspection, pH determination, and high-performance liquid chromatography were performed in duplicate on samples removed at zero, two, and four hours. No change in pH or appearance occurred throughout the study. All drug concentrations remained above 90% of the initial concentration in each combination. Labetalol hydrochloride 1.0 mg/mL and dobutamine 2.5 mg/mL (as the hydrochloride salt), dopamine hydrochloride 1.6 mg/mL, morphine sulfate 0.5 mg/mL, nitroglycerin 0.2 mg/mL, or ranitidine 0.6 mg/mL (as the hydrochloride salt) in 5% dextrose injection were stable and compatible for up to four hours at 20-25 degrees C during simulated Y-site injection.

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Of 84 initially treated patients, 73 entered the maintenance study. The percentage of asymptomatic patients after 90-day and 210-day treatment were 97% and 81.5%, for rabeprazole and 74.3% and 62.3%, for ranitidine, respectively. After 32 weeks, the relapse rates of esophagitis were 21.3% in the rabeprazole group and 62.9% in the ranitidine group (RR: 0.405, 95% CI: 0.215-0.766).

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Ranitidine bismuth citrate (RBC) is a new chemical entity for the treatment of peptic ulcer disease.

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A total of 15,495 patients registered with eight general practitioners in seven general practices in Dundee, UK.

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Serum samples for measurement of ranitidine concentrations were collected at 2, 6, and 12 hrs after the fifth dose of oral ranitidine. Patients were monitored for upper gastrointestinal bleeding. All patients had therapeutic serum ranitidine concentrations at 2 and 6 hrs, while 88% of patients had therapeutic levels at 12 hrs.

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Fewer patients undergoing omeprazole therapy required redilatation compared with those on ranitidine (43 of 143 [30%] vs. 66 of 143 [46%] by 12 months; P < 0.01), and patients in the omeprazole group needed fewer redilatations during the year (0.48 vs. 1.08; P < 0.01). On completion, symptom relief favored omeprazole: 76% of patients in the omeprazole group were free of dysphagia (compared with 64% in the ranitidine group; P < 0.05); 83% were able to accept a normal diet (69%; P < 0.01); and 65% were completely asymptomatic (43%; P < 0.001).

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A 56 year old female with acute pancreatitis and a known allergy to metronidazole and buscopan developed an anaphylaxis few minutes following the injection of ranitidine for epigastric discomfort. She went on to develop anaphylactic shock and a cardiorespiratory arrest.

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The effect of pretreatment with ranitidine, an antacid, on the absorption of AS-924, a novel prodrug-type cephem antibiotic derived from ceftizoxime (CTIZ), was examined in eight healthy adult male volunteers by the cross-over method, using cefteram-pivoxil (CTER-PI) as the control drug. The C(max) and area under the concentration (AUC) values and cumulative urinary excretion rate (0-24 h) of cefteram (CTER) after administration of CTER-PI decreased by 32, 38 and 37%, respectively, in the ranitidine pretreatment group whereas those of AS-924 were not affected by the antacid. The urinary levels of pivaloyl-carnitine determined to evaluate the solubility of these antibiotics in the gastrointestinal tract suggested that this was not affected by ranitidine. These results indicate that the absorption of CTER-PI was affected by pretreatment with ranitidine largely due to inactivation of this antibiotic in the gastrointestinal tract at high pH rather than to a decrease in solubility. In contrast, isomerization of AS-924 was hardly induced by the elevation of pH, thus demonstrating that AS-924 was less likely to be affected by pretreatment with antacids.

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A program in which pharmacists were authorized to change parenteral histamine H2-receptor antagonist (H2RA) therapy to the oral route without first contacting the prescriber was evaluated on cost and appropriateness of use of the parenteral route. Parenteral therapy was received by 264 and 244 patients in the study and comparison groups, respectively. Length of parenteral H2RA therapy was less in the study group (4.8 vs. 7.5 d) as was length of total (parenteral + oral) therapy (8.4 vs. 12.1 d). Parenteral H2RA drug acquisition savings were $6225 in the six-week study period or $53,950 when annualized. Decreased oral therapy contributed additional savings. There was a significant decrease in the number of inappropriate parenteral doses of ranitidine per patient, the drug used in more than 80 percent of the patients. In addition to the direct effect of pharmacists' interventions, there appeared to be an indirect effect of the program, as physicians initiated route of administration changes on their own.

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We evaluated 274 VLBW infants: 91 had taken ranitidine and 183 had not. The main clinical and demographic characteristics did not differ between the 2 groups. Thirty-four (37.4%) of the 91 children exposed to ranitidine and 18 (9.8%) of the 183 not exposed to ranitidine had contracted infections (odds ratio 5.5, 95% confidence interval 2.9-10.4, P < .001). The risk of NEC was 6.6-fold higher in ranitidine-treated VLBW infants (95% confidence interval 1.7-25.0, P = .003) than in control subjects. Mortality rate was significantly higher in newborns receiving ranitidine (9.9% vs 1.6%, P = .003).

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Colloidal bismuth subcitrate (CBS; DeNol) has been studied in clinical trials investigating the treatment of duodenal and gastric ulcer, non-ulcer dyspepsia, duodenitis, non-steroidal anti-inflammatory drug (NSAID)-induced disease, and Helicobacter pylori-induced gastroduodenitis. Healing rates for duodenal ulcer with CBS are significantly better than with placebo and are similar to results obtained with cimetidine or ranitidine. CBS is significantly better in the treatment of duodenal ulcer resistant to standard doses of H2 antagonists than increased doses of H2 antagonists. Duodenal ulcer relapse at 12 months after initial healing with CBS is significantly less than with H2-antagonist therapy. Ulcer healing with CBS is not influenced by smoking. H. pylori eradication with CBS appears to have little effect in ulcer healing but is of major importance in preventing ulcer relapse. CBS is effective in combination with antibiotics in eradicating H. pylori-associated gastritis. In gastric ulcer disease CBS therapy resulted in significant healing advantages over placebo and was comparable to treatment with cimetidine and sucralfate. CBS has been shown to be effective in the treatment of erosive duodenitis. The role of CBS in treatment of non-ulcer dyspepsia and NSAID-induced damage awaits further clinical studies.

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To test the eradication rate of Helicobacter pylori by ranitidine bismuth citrate-based triple therapy, and evaluate the symptomatic response of Helicobacter pylori eradication therapy for non-ulcer dyspepsia.

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To evaluate the effect of Bicitra (Willen Drug Company, Baltimore, Maryland), a commercial preparation of sodium citrate and metoclopramide, on gastric contents 150 elective outpatients allocated into six groups with 25 patients in each group were studied. Patients in Group 1 served as controls. Patients in Groups 2, 3, 5, and 6 received Bicitra, po, either 15 ml (Groups 2 and 5) or 30 ml (Groups 3 and 6). In addition, patients in Groups 5 and 6 also received metoclopramide 10 mg, iv; Group 4 patients received metoclopramide 10 mg, iv. Eighty-eight per cent of patients in the control group had a gastric pH less than or equal to 2.5, while 36% had a gastric content volume greater than or equal to 25 ml with pH less than or equal to 2.5. Bicitra, 15 ml and 30 ml, po, increased mean gastric pH and decreased the proportion of patients with a gastric pH less than or equal to 2.5 to 32 and 16%, respectively, in Groups 2 and 3. However, Bicitra 15 ml and 30 ml, increased the mean gastric volume in Group 3 and also increased the proportion of patients with a gastric volume greater than or equal to 25 ml to 56% in Group 2 and 84% in Group 3. The addition of metoclopramide 10 mg, iv, to Bicitra reduced the proportion of patients with a gastric volume greater than or equal to 25 ml in Groups 5 and 6 to 28 and 36%, respectively. Metoclopramide (Group 6) independently reduced mean gastric volume (15.6 ml vs. 32.7 ml) and the proportion of patients with a gastric volume greater than or equal to 25 ml (20% vs. 36%). Bicitra and metoclopramide combination significantly reduced the proportion of patients with gastric contents greater than or equal to 25 ml with pH less than or equal to 2.5.

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We report four chronically constipated female gastroesophageal reflux disease-patients with reflux symptoms and an increased number of reflux episodes in combined esophageal pH and multichannel impedance monitoring treated with prucalopride (2mg per day). Symptoms were persistent to proton pump inhibitors and ranitidine. Gastroesophageal reflux was detected by pH or multichannel impedance (MII) monitoring. Numbers of all reflux episodes as well as non-acid reflux episodes were reduced in all of our patients. The objective findings were concordant with subjective reports of symptom relief. There were no major adverse events in any patient during therapy with prucalopride.

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The results suggest that gastrin stimulates acid secretion by releasing histamine from ECL cells. Vagally induced acid secretion is also dependent on a histaminergic pathway but not on ECL-cell histamine.

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Famotidine and ranitidine in over-the-counter doses have a similar, sustained, effect on post-prandial nocturnal intragastric acidity in healthy subjects lasting up to 12 h after oral dosing.

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The overall unadjusted study odds ratio for VAP was 0.82 (P = .21) representing a trend toward less pneumonia with sucralfate compared with ranitidine. The odds ratio adjusted for adjudication pair was 0.85 (P = .27). The proportion of charts adjudicated as VAP positive among pairs ranged from 50% to 92%; crude agreement between readers in each pair varied from 50% to 82%. When adjudicators disagreed, the final consensus was split evenly between the two adjudicators' initial opinions in two pairs; in the other two pairs, the final decision reflected one dominant initial opinion. Personnel time to adjudicate all patients with a suspicion of VAP was 74 days.

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Cimetidine, an H2-receptor antagonist, is one of the most commonly prescribed drugs in the world. It has been reported to increase blood alcohol concentrations in drinking individuals. To determine if this increase could be due to inhibition of alcohol dehydrogenase activity, the effect of the drug on ethanol oxidation by gastric sigma sigma alcohol dehydrogenase and liver beta 2 beta 2, pi pi, and chi chi alcohol dehydrogenase isoenzymes was observed. Cimetidine inhibited all isoenzymes studied except chi chi; the chi chi isoenzyme showed no inhibition up to 5 mM cimetidine. Inhibition of the alcohol dehydrogenase isoenzymes by the H2-receptor antagonists nizatidine, ranitidine, and famotidine was negligible. Docking simulations with the beta 2.NAD+.4-iodopyrazole X-ray structure indicated that cimetidine fit well into the substrate binding site. The substitution on the thiazole ring of nizatidine, however, prevented docking into the binding site. Cimetidine inhibition of ethanol oxidation by sigma sigma and beta 2 beta 2 was competitive with varied ethanol, exhibiting Ki values of 2.8 +/- 0.4 mM and 0.77 +/- 0.07 mM, respectively. Cimetidine inhibition of ethanol oxidation by pi pi was noncompetitive with varied ethanol (Ki = 0.50 +/- 0.03 mM). Inhibition of ethanol oxidation by sigma sigma and beta 2 beta 2 with varied NAD+ was competitive. These results, together with the cimetidine inhibition kinetics of acetaldehyde reduction by sigma sigma and beta 2 beta 2, with either varied NADH or varied acetaldehyde, are consistent with cimetidine binding to two enzyme species. These species are free enzyme and the productive enzyme.NAD+ complex.

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The results of this pilot study revealed that among the outpatients suffering from rheumatic diseases, the number of females was double as high as the number of males, that these patients were of the mean age of 70 years, and that their diseases lasted longer than five years. Gastric complains such as nausea and gastric pain of mild intensity were the most often adverse effects of NSAIDs reported by our patients. It could be the consequence of the predominant use of diclofenac and ibuprofen, NSAIDs with mild to moderate ulcerogenic potential, as well as the concomitant use of H2-receptor antagonists.

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We have previously shown that sensory nerve peptides contribute to the pathogenesis of pulmonary hypersensitivity reactions (HSRs) to paclitaxel in rats. Moreover, pemirolast, an antiallergic agent, reverses the HSRs to paclitaxel, although the mechanism is considered to result from the blockade of paclitaxel-induced release of sensory peptides, rather than the inhibition of histamine release. In the present study, we investigated the preventive effect of pemirolast against acute HSRs in a total of 84 patients who undertook postoperative paclitaxel plus carboplatin chemotherapy every 4 weeks for ovarian cancer. Patients were assigned to receive oral lactose (placebo) or pemirolast (10 mg), 2 hr before paclitaxel infusion. All patients received conventional premedication, including oral diphenhydramine, intravenous ranitidine and intravenous dexamethasone, 30 min before paclitaxel infusion. The HSRs that led to the discontinuance of paclitaxel infusion (grade>or=2) occurred in 5 of 42 patients in placebo group, whereas none of pemirolast-treated 42 patients showed any signs of HSRs. Plasma histamine concentrations were not changed after paclitaxel infusion in either group. Our present findings suggest that pemirolast is potentially useful for prophylaxis of paclitaxel-induced HSRs. In this respect, the use of pemirolast as premedication is expected to be beneficial to the safety management in patients who undergo chemotherapy containing paclitaxel.

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We studied the effects of preanesthetic ranitidine on gastric contents in 60 outpatients scheduled for elective surgery, with random allocation into three groups of 20 patients each. Patients in group 1 did not receive ranitidine and served as controls. Patients in groups 2 and 3 received ranitidine orally, 150 and 300 mg, respectively, one to five hours before induction of anesthesia. In the control group, mean pH and volume of gastric contents were 1.90 and 27.7 ml respectively. Ninety percent of the control subjects had gastric pH less than or equal to 2.5, and 65% of the patients had pH less than or equal to 1.8; 65% of the patients had gastric volumes of 20 ml or greater. Ranitidine in 150 and 300 mg doses markedly raised mean gastric pH to 6.40 and 5.87 respectively and reduced the proportion of patients with gastric pH less than or equal to 2.5 to 10% in group 2 and 0% in group 3. Mean gastric volume and proportion of patients with volume greater than or equal to 20 ml were significantly reduced in both treatment groups. Proportions of patients with combination of pH less than or equal to 2.5 and volume greater than or equal to 20 ml were significantly low in both treatment groups, as there was only one patient in group 2 and none in group 3 with both low pH and high volume. With respect to reduction of gastric acidity and volume, 300 mg of ranitidine had no advantage over 150 mg.

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Studies evaluating RBC plus two antibiotics were considered. For the meta-analysis, randomized controlled trials comparing PPI vs. RBC plus two antibiotics for 1 week were included.

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Thirteen percent of older veterans with a CrCl of 30 to 49 mL/min and 32% of those with a CrCl of 15 to 29 mL/min received one or more drugs that were contraindicated or prescribed at an excessive dose given the individual's level of renal function. The strongest risk factor for renally inappropriate prescribing was number of medications used; the risk of receiving renally inappropriate medications was 5.5 times as high (95% confidence interval = 5.1-5.9) in older adults taking 10 or more medications as in those taking one to three medications. Ranitidine, allopurinol, and metformin together accounted for 76% of renally misprescribed medications in individuals with a CrCl of 30 to 49 mL/min. Glyburide, ranitidine, gemfibrozil, carvedilol, and allopurinol accounted for 47% of renally misprescribed drugs for individuals with a CrCl of 15 to 29 mL/min.

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The present study was aimed to investigate the effects of microinjection of histamine and its H1, H2 and H3 receptor antagonists, mepyramine, ranitidine and thioperamide, respectively, into the anterior cingulate cortex (ACC) on pain-related behaviors induced by formalin in rats.

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Histamine is a potent mediator in allergic inflammatory processes and is released by basophils and mast cells. The aim of this study was to investigate the effect of histamine on in vitro migration of human fetal lung fibroblasts (HFL-1) to human plasma fibronectin (HFn), a chemoattractant. Using the blindwell chamber technique, histamine alone had no chemotactic activity. However, histamine augmented HFn-induced HFL-1 migration at concentrations ranging between 0 and 10(-7) M (290.6 +/- 20.8%) (P < 0.05). The concentration-response was bell-shaped. The effect of histamine increased with time. The stimulatory effect of histamine on HFL-1 migration was inhibited by an H4 receptor antagonist, JNJ7777120 (10(-5) M). Histamine's effect was also inhibited by pertussis toxin (50 ng/ml), showing that the effect was mediated by the H4 receptor. This study demonstrated that histamine has the potential to stimulate human lung fibroblast migration, and thus may contribute to regulation of wound healing and the development of fibrotic disorders of the lung.

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zantac 150 tablets 2015-03-03

Elderly patients with pyrosis buy zantac symptoms severe enough to require upper gastrointestinal endoscopy have gastroesophageal reflux disease with more esophageal mucosal disease (erosive esophagitis, Barrett's esophagus) than patients < 60 yr, and like younger patients, may require markedly increased doses of ranitidine as large as 2400 mg/d for effective therapy.

zantac 75 generic 2017-10-24

In a randomized, endoscopically controlled trial, the effects of colloidal bismuth subcitrate (CBS) tablets on the healing of chronic duodenal ulcers were compared with those of ranitidine (R). 38 patients were originally allocated to the CBS group and 37 to ranitidine. There were 5 dropouts in each group. Of 33 patients given CBS, 25 (75%) showed complete ulcer healing by 4 weeks and 30 (91%) by 8 weeks. Of the 32 patients given ranitidine, 28 (87%) showed complete ulcer healing by 4 weeks and 30 (94%) by 8 buy zantac weeks. There was no significant difference between these results. Symptom resolution was similar in both groups and no significant adverse effects were noted.

zantac 20 mg 2015-04-11

Corticosteroids and cytostatic drugs possess a documented lesive action on upper digestive mucosa, making epigastric pain and/or pyrosis common complaints among patients on antitumor treatment. The selective antimuscarinic pirenzepine and the H2-receptor antagonist ranitidine buy zantac were tested against the ulcerogenic action of antiblastic chemotherapy. Thirty-eight patients affected with malignant lymphoproliferative disorders were endoscopically examined and the endoscopic pictures were quantified by using an arbitrary score. According to a double-blind randomized sequence, 19 out of the 38 patients received pirenzepine 100 mg/die/p.o. and the other 19 received ranitidine 300 mg/die/p.o. along with antitumoral therapy for periods of 3-6 months. Seven patients died of hematologic complications before ending the treatment. In the 31 surviving patients (13 pirenzepine- and 18 ranitidine-treated) a second endoscopic examination was performed at the end of the treatment and the lesion score repeated. No significant difference was found between initial and final scores in both groups. The antisecretive action of the two drugs may account for their effectiveness, but other mechanisms such as cytoprotection cannot be ruled out.

zantac 450 mg 2017-12-26

The effects on prolactin secretion of histamine H2-receptor antagonists infused intracerebroventricularly were studied in urethane anaesthetized male rats. A dose of 1.6 mumol cimetidine stimulated basal prolactin secretion and did not affect the histamine-induced release, whereas 0.4 mumol cimetidine inhibited basal and histamine-stimulated prolactin secretion. 0.1 mumol cimetidine had no effect. The more potent H2-receptor antagonist ranitidine at doses of 0.1, 0.4, 1.6 mumol had no effect on basal prolactin secretion, whereas 0.4 and 1.6 mumol inhibited buy zantac the histamine-stimulated secretion completely. SKF-92408, a compound resembling cimetidine in chemical structure but devoid of H2-receptor antagonist activity, stimulated basal prolactin secretion at a dose of 1.6 mumol, but had no effect on the histamine-induced release or at a dose of 0.4 mumol. The H2-receptor antagonists metiamide and oxmetidine (1.6 mumol) stimulated basal prolactin secretion and did not prevent the response to histamine. A dose of 0.4 or 1.6 mumol imidazole (the ring structure contained in cimetidine, SKF-92408, metiamide, and oxmetidine) had no effect on basal or histamine-stimulated prolactin secretion. The findings indicate that cimetidine stimulates prolactin secretion by a non-specific action when infused centrally at high doses. In contrast, when infused at lower doses cimetidine inhibits the basal and histamine-stimulated secretion by blockade of H2-receptors. The prolactin-stimulatory action of cimetidine was not due to an H2-agonist effect, since ranitidine did not prevent the response. Cimetidine did not stimulate prolactin secretion via an effect on the dopaminergic system, since the drug had no effect on the dopamine concentration in hypophysial portal blood or in hypothalamic tissue and since inhibition of the dopamine synthesis by alpha-methyl-p-tyrosine did not prevent the cimetidine-induced prolactin release.

zantac po dosing 2016-09-20

There were 3 groups of rats examined: 1) a chronic gastroesophageal reflux buy zantac rat group, which was created by a partial gastric outlet obstruction; 2) a sham group; and 3) a ranitidine treated group. Serial sections ofbrainstems of all groups were cut and NADPH-d staining, which selectively stains the nitric acid synthase-containing neurons, was done.

zantac chewable tablets 2016-03-07

Children undergoing general anesthesia are at increased risk of severe aspiration pneumonitis. Cimetidine and ranitidine, specific histamine (H2-receptor) antagonists, when given 1-3 h preoperatively markedly reduce the acidity and volume of gastric content. A newer compound, famotidine, is a more specific antagonist with no inhibitory effect on the drug metabolizing microsomal enzyme systems of the liver (cytochrome P-450), in contrast to cimetidine. An additional clinical advantage is a possible longer duration of action. In order to evaluate these potential advantages we studied the effects of preanesthetic oral famotidine on gastric fluid pH and volume in 4 groups in a random manner. METHODS. With parental consent, 107 infants and children (ASA I status, 4 months to 14 years old, NPO buy zantac for at least 6 h) received either no famotidine (n = 29) or 0.15 mg/kg (n = 27), 0.3 mg/kg (n = 25) or 0.6 mg/kg (n = 26) famotidine at 7.00 a.m. Following induction by mask with nitrous oxide/oxygen (N2O/O2) and enflurane (E) or i.v. thiopental, intubation was performed in all patients. Anesthesia was maintained with N2O/O2 and E. A orogastric double-lumen tube was passed into the stomach, and the gastric content was aspirated in a uniform manner. Gastric volume was recorded and pH values were measured with pH paper. RESULTS. In the control group, 28 of 29 patients (97%) had a pH less than 2.5, 18/29 (62%) had a gastric volume greater than 0.4 ml/kg and 17/29 (59%) had a pH less than 2.5 and gastric volume greater than 0.4 ml/kg, meaning an increased risk of pneumonitis if the child aspirates the gastric content. Famotidine administration was effective between 1.5 and 6 h after oral administration. Preoperative famotidine application produces pH values of gastric contents higher than 2.5 in all dosage groups (84%, 94%, 75%), and these differences were highly significant (P less than 0.001), whereas the gastric volume reduction with these doses was not significant. The incidence of pH less than 2.5 and volume of gastric contents exceeding 0.4 ml/kg did not vary with the different doses of famotidine. As there were no measurable differences in the effect of famotidine, we recommend that children at high risk of pulmonary aspiration receive 0.15 mg/kg famotidine orally at least 1.5 h but not later than 6 h before induction.

zantac overdose infant 2017-10-03

Histamine is widely distributed in the lungs and increases capillary permeability and P-selectin expression. To observe the role of histamine in acute lung injury (ALI), we measured the histamine and protein concentrations and cell numbers in the bronchoalveolar lavage (BAL) of LPS-induced ALI in rats. We instilled LPS (3 mg/kg) intratracheally, in conjunction with the intravenous histamine receptor antagonists (mepyramine, a H1-receptor antagonist, or ranitidine, a H2-receptor antagonist). LPS increased protein concentration and neutrophil numbers in the BAL as well as myeloperoxidase (MPO) activity in lungs after 6 h. LPS also increased histamine concentration in BAL after 2 h. Mepyramine and ranitidine attenuated the increased histamine concentrations. Total cell number in the BAL and MPO activity in buy zantac the lungs were significantly decreased and neutrophil numbers and protein concentration in the BAL seemed to decrease with the administration of ranitidine at 6 h. In conclusion, endogenous histamine might be involved in the recruitment of neutrophils and protein leaks in LPS-induced ALI via the H2 receptors.

zantac drug 2016-12-14

A comparison was made of the antisecretory activity of orally administered nizatidine and ranitidine by measuring intragastric pH under basal conditions and during and after pentagastrin stimulation. Intragastric pH values were measured with a bipolar glass electrode in 10 patients with healed duodenal ulcers treated with nizatidine or ranitidine according to a randomized single-blind design. The antisecretory activity of the two drugs was similar during the 4 h of monitoring following drug administration. Nizatidine, however, showed a more rapid inhibitory action than ranitidine, producing a significantly greater increase in pH with respect to basal values during pentagastrin infusion. In the period following infusion the pH values observed with ranitidine were higher than with nizatidine, but not significantly so. Under these experimental conditions, therefore, the buy zantac antisecretory activity of nizatidine was shown to be more rapid than that of ranitidine and equally effective.

zantac dosing child 2015-03-02

The older proton buy zantac pump inhibitor (PPI) omeprazole and the newer PPIs lansoprazole, rabeprazole, and pantoprazole are approved for the acute and maintenance treatment of gastroesophageal reflux disease (GERD).

zantac 50 mg 2015-03-14

The prophylaxis of stress ulcers in intubated patients treated with antacids and ranitidine provoked higher gastric pH and an increase in gastric colonization in comparison buy zantac to that observed with sucralfate. No significant differences were observed in the frequency of pneumonia by PMV diagnosed by BBTC.

zantac kids dosage 2016-12-22

Cumulative direct treatment costs per 100 patients with duodenal ulcer disease who were positive buy zantac for H pylori.

zantac and alcohol 2017-07-22

The effects of eight-week ranitidine treatment on changes in plasma gastrin, histamine and serotonin levels, and in intragastric pH and urinary 5-hydroxyindoleacetic acid in duodenal ulcer patients were studied. Elevated plasma gastrin and histamine levels, as well as intragastric pH were found buy zantac after four weeks of ranitidine treatment, only in patients whose ulcers had healed. Plasma serotonin and urinary 5-hydroxyindoleacetic acid levels decreased as drug treatment continued, and the falls were similar in patients whose ulcers healed or did not. It is suggested that the increases in plasma gastrin, histamine and serotonin levels could be due to gastric and duodenal acid reductions by ranitidine. However, the possibility of a direct action of the drug on their release is yet to be excluded.

zantac generic name 2016-02-13

In the last few years, several drugs have been proposed for the healing of peptic ulcers H2 receptor antagonists are probably the buy zantac reference-drugs for their efficacy and safety. Acute treatment of peptic ulcer with cimetidine, ranitidine or famotidine gives a high healing rate: from 60% to 90%, depending on the location of the ulcer and the drug used. However, relapse after short-term treatment still remains frequent, and prophylaxis of recurrence must be decided. Long-term treatment with antisecretory drugs could be dangerous for changes of the gastric system, with nitrites and nitro-compounds occurrence, and for the risk of frequent relapses. Therefore, the role of mucus-barrier drugs and surgery must be reconsidered.

8 mg zantac 2015-03-28

Ranitidine did not change gastric volume before the meal, nor at 0 h or 1 h after it. Furthermore, ranitidine did not influence gastric retention of meal components buy zantac after 0.5 h and 1 h.

zantac 2 tablets 2015-07-07

The combined therapy with amoxycillin, metronidazole, furoxone and ranitidine is highly effective in both Hp eradication and Zocor 80 Mg prevention of DU recurrence.

zantac generic recall 2017-10-04

Ranitidine hydrochloride (an H2-receptor-blocking drug which does not contain the imidazole nucleus of histamine) powerfully inhibited nocturnal and pentagastrin-stimulated gastric secretion in fifteen Buy Cleocin patients with duodenal ulceration. The drug is satisfactorily absorbed and therefore warrants clinical trial.

zantac brand name 2015-01-04

Increasing evidence suggests that a continuous release of histamine from mast cells occurs in the airways of asthmatic patients and that histamine may modulate functions of other inflammatory cells such as macrophages. In Cytoxan Lupus Dosage the present study histamine (10(-9)-10(-6) M) increased in a concentration-dependent fashion the basal release of beta-glucuronidase (EC(50) = 8.2 +/- 3.5 x 10(-9) M) and IL-6 (EC(50) = 9.3 +/- 2.9 x 10(-8) M) from human lung macrophages. Enhancement of beta-glucuronidase release induced by histamine was evident after 30 min and peaked at 90 min, whereas that of IL-6 required 2-6 h of incubation. These effects were reproduced by the H(1) agonist (6-[2-(4-imidazolyl)ethylamino]-N-(4-trifluoromethylphenyl)heptane carboxamide but not by the H(2) agonist dimaprit. Furthermore, histamine induced a concentration-dependent increase of intracellular Ca(2+) concentrations ([Ca(2+)](i)) that followed three types of response, one characterized by a rapid increase, a second in which [Ca(2+)](i) displays a slow but progressive increase, and a third characterized by an oscillatory pattern. Histamine-induced beta-glucuronidase and IL-6 release and [Ca(2+)](i) elevation were inhibited by the selective H(1) antagonist fexofenadine (10(-7)-10(-4) M), but not by the H(2) antagonist ranitidine. Inhibition of histamine-induced beta-glucuronidase and IL-6 release by fexofenadine was concentration dependent and displayed the characteristics of a competitive antagonism (K(d) = 89 nM). These data demonstrate that histamine induces exocytosis and IL-6 production from human macrophages by activating H(1) receptor and by increasing [Ca(2+)](i) and they suggest that histamine may play a relevant role in the long-term sustainment of allergic inflammation in the airways.

zantac tablets 150mg 2016-08-13

All patients who were referred to the gastroenterology clinic at the University Health Center to evaluate their heartburn and who met the inclusion criteria were Vantin Tablets included in the present study. Symptomatic and endoscopic evaluations were carried out and then they were started on the proton pump inhibitor lansoprazole to achieve symptomatic control. Step-down therapy was carried out for these patients, provided their symptoms remained controlled. At the end of the study symptomatic and endoscopic outcomes were evaluated.

zantac 75 dosage 2015-01-07

Functional role of endothelial alpha(2)-adrenoceptor in coronary circulation remains unclear. Clonidine, an agonist of alpha(2)-adrenoceptors, was reported to induce coronary vasodilatation via stimulation of endothelial alpha(2)-adrenoceptors or coronary vasoconstriction involving vascular smooth muscle alpha(2)-adrenoceptors. Moreover, H(2) receptor-dependent responses to clonidine were described. Here, we reassess the contribution of endothelial alpha(2)-adrenoceptor and H(2) receptors to coronary flow and contractility responses induced by clonidine in the isolated guinea pig heart. We found that clonidine (10(-9) - 10(-6) M) produced concentration-dependent coronary vasoconstriction without a significant change in contractility. This response was inhibited by the alpha(1)/alpha(2)-adrenoceptor antagonist - phentolamine (10(-5) M) and the selective alpha(2)-adrenoceptor antagonist yohimbine (10(-6) M), but it was not changed by the selective alpha(1)-adrenoceptor antagonist prazosin (10(-6) M). In the presence of nitric oxide synthase inhibitor, L-NAME (10(-4) M) the clonidine-induced vasoconstriction was potentiated. Clonidine at high concentrations of 10(-5) - 3 x Cleocin Generic 10(-5) M produced coronary vasodilatation, and an increase in myocardial contractility. These responses were abolished by a selective H(2)-receptor antagonist, ranitidine (10(-5) M), but not by phentolamine (10(-5) M). We conclude that in the isolated guinea pig heart, clonidine-induced vasoconstriction is mediated by activation of smooth muscle alpha(2)-adrenoceptors whereas clonidine-induced coronary vasodilatation is mediated by activation of vascular H(2) histaminergic receptors. Accordingly, endothelial alpha(2)-adrenoceptors does not seem to play a major role in coronary flow response induced by clonidine.

zantac dosage child 2015-11-12

The aim of this study was to determine the one-year outcome of an eradication therapy with ranitidine bismuth citrate Rheumatica Prednisone Dosage and antibiotics in Helicobacter pylori-positive duodenal ulcer patients in respect to ulcer and Helicobacter pylori relapse rates.