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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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Etravirine (formerly TMC125) is a non-nucleoside reverse transcriptase inhibitor (NNRTI) with activity against wild-type and NNRTI-resistant strains of HIV-1. Etravirine has been approved in several countries for use as part of highly active antiretroviral therapy in treatment-experienced patients. In vivo, etravirine is a substrate for, and weak inducer of, the hepatic cytochrome P450 (CYP) isoenzyme 3A4 and a substrate and weak inhibitor of CYP2C9 and CYP2C19. Etravirine is also a weak inhibitor of P-glycoprotein. An extensive drug-drug interaction programme in HIV-negative subjects has been carried out to assess the potential for pharmacokinetic interactions between etravirine and a variety of non-antiretroviral drugs. Effects of atorvastatin, clarithromycin, methadone, omeprazole, oral contraceptives, paroxetine, ranitidine and sildenafil on the pharmacokinetic disposition of etravirine were of no clinical relevance. Likewise, etravirine had no clinically significant effect on the pharmacokinetics of fluconazole, methadone, oral contraceptives, paroxetine or voriconazole. No clinically relevant interactions are expected between etravirine and azithromycin or ribavirin, therefore, etravirine can be combined with these agents without dose adjustment. Fluconazole and voriconazole increased etravirine exposure 1.9- and 1.4-fold, respectively, in healthy subjects, however, no increase in the incidence of adverse effects was observed in patients receiving etravirine and fluconazole during clinical trials, therefore, etravirine can be combined with these antifungals although caution is advised. Digoxin plasma exposure was slightly increased when co-administered with etravirine. No dose adjustments of digoxin are needed when used in combination with etravirine, however, it is recommended that digoxin levels should be monitored. Caution should be exercised in combining rifabutin with etravirine in the presence of certain boosted HIV protease inhibitors due to the risk of decreased exposure to etravirine. Although adjustments to the dose of clarithromycin are unnecessary for the treatment of most infections, the use of an alternative macrolide (e.g. azithromycin) is recommended for the treatment of Mycobacterium avium complex infection since the overall activity of clarithromycin against this pathogen may be altered when co-administered with etravirine. Dosage adjustments based on clinical response are recommended for clopidogrel, HMG-CoA reductase inhibitors (e.g. atorvastatin) and for phosphodiesterase type-5 inhibitors (e.g. sildenafil) because changes in the exposure of these medications in the presence of co-administered etravirine may occur. When co-administered with etravirine, a dose reduction or alternative to diazepam is recommended. When combining etravirine with warfarin, the international normalized ratio (INR) should be monitored. Systemic dexamethasone should be co-administered with caution, or an alternative to dexamethasone be found as dexamethasone induces CYP3A4. Caution is also warranted when co-administering etravirine with some antiarrhythmics, calcineurin inhibitors (e.g. ciclosporin) and antidepressants (e.g. citalopram). Co-administration of etravirine with some antiepileptics (e.g. carbamazepine and phenytoin), rifampicin (rifampin), rifapentine or preparations containing St John's wort (Hypericum perforatum) is currently not recommended as these are potent inducers of CYP3A and/or CYP2C and may potentially decrease etravirine exposure. Antiepileptics that are less likely to interact based on their known pharmacological properties include gabapentin, lamotrigine, levetiracetam and pregabalin. Overall, pharmacokinetic and clinical data show etravirine to be well tolerated and generally safe when given in combination with non-antiretroviral agents, with minimal clinically significant drug interactions and no need for dosage adjustments of etravirine in any of the cases, or of the non-antiretroviral agent in the majority of cases studied.

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The probability of recurrence for patients who received triple therapy plus ranitidine was significantly lower than that for patients who received ranitidine alone: for patients with duodenal ulcer, 12% (95% CI, 1% to 24%) compared with 95% (CI, 84% to 100%); for patients with gastric ulcer, 13% (CI, 4% to 31%) compared with 74% (44% to 100%). Fifty percent of patients who received ranitidine alone for healing of duodenal or gastric ulcer had a relapse within 12 weeks of healing. Ulcer recurrence in the triple therapy group was related to the failure to eradicate H. pylori and to the use of nonsteroidal anti-inflammatory drugs.

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Overall, there was a 15%, 21% and 23% decrease in the number of patients in the RBC, L and O programs, respectively, with ulcers among H. pylori cleared/eradicated patients post-treatment compared with patients with persistent infection. Among patients who did not have cleared/eradicated H. pylori in the RBC and O programs, where antisecretory agents were continued beyond the antimicrobial treatment period, the number of ulcers was lower in the antisecretory plus antimicrobial subgroups compared with the antimicrobial alone subgroups (37% vs. 46% for RBC and 33% vs. 42% for O). Among patients with cleared/eradicated H. pylori, the number of patients with ulcers in the antimicrobial alone subgroups and antisecretory plus antimicrobial subgroups were similar within each program. Antimicrobials alone had significantly lower rates of ulcers among patients with cleared/eradicated H. pylori as compared with patients without clearance/eradication.

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during 2006 and 2007 a total of 49 patients in the case group and 50 patients in the control group were included in the study. A serie of qualitative variables comparing the two groups to determine their association were analyzed.

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Cell mediated immunity was tested 3 days before, and 4 days after, operation by reactions to 7 recall antigens (Multitest, Merieux). 21 patients were randomly allocated to receive ranitidine 100 mg twice daily intravenously from the day before operation until the third postoperative day.

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To evaluate the influence of cimetidine, ranitidine, famotidine, and placebo on cardiac performance as determined by echocardiography.

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Treatment with ranitidine dose-dependently increased protein content in the gastric vesicular fraction purified from the gastric mucosa without changing total protein content. Ranitidine also increased the content of a 94,000-dalton protein, the catalytic subunit of H+,K(+)-ATPase. On the other hand, ranitidine did not affect the specific activity of the enzyme (mumol/min/mg of the gastric vesicular protein). Since gastric vesicles in the fasting state mainly consist of the tubulovesicular membrane, these results suggest that ranidine administration increases total tubulovesicular H+,K(+)-ATPase content (mumol/min/rat) by increasing the number of tubulovesicles per parietal cell. The ranitidine-induced increase in total tubulovesicular H+,K(+)-ATPase activity was still evident 1 week after treatment and returned to control level 1 month later.

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Helicobacter pylori was eliminated in 14 of 20 children studied. All these children had an important improvement of recurrent abdominal pain.

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Patients of group I and II had similar demographic and clinical characteristics. The overall proportion of eradication of H. pylori infection was 81.8% in group I and 78.6% in group II (P = N.S.) as judged from negative bacterial findings by means of an urease test, specific culture and histology after modified Giemsa stain. Ulcer healing was observed in all patients after a maximum duration of 10 weeks. Ten patients on triple therapy and only one patient on omeprazole plus amoxycillin (45.5% vs. 3.6%; P < 0.001) complained of side effects without necessity of discontinuation of the study medication in either group. Twenty patients (group I: n = 10; group II: n = 10) with relapsing duodenal ulcer disease and successful cure were prospectively followed for one year without any evidence of ulcer relapse or H. pylori re-infection.

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Gastric mucosal cells were isolated from human mucosa obtained at surgery. H+ production was indirectly estimated by 14C aminopyrine (AP) uptake. The maximal response to histamine occurred after 30 min of incubation whereas intrinsic factor (IF) secretion was maximal after only 7.5 to 15 min. According to the concentration response curve 10(-4) mol/1 histamine proved to be the most effective concentration, the response to which was completely inhibited by ranitidine. Carbachol, dibutyryl cAMP and IMX also enhanced AP uptake, IMX being even more powerful than histamine. Carbachol and IMX failed to potentiate the response to histamine. Parietal cell fractions enriched by a Percoll density gradient revealed a pronounced background stimulation so that additional stimulation by test agents was less effective than in non-fractionized cells.

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Nontoxic doses of the histamine H2 antagonists ranitidine, cimetidine, lamtidine and mifentidine rapidly and reversibly increased tyrosinase activity in an amelanotic human melanoma cell line (MM96L) with low constitutive activity. The H2 antagonists, famotidine and MGTI, and the imidazol(in)e receptor ligand clonidine had no effect either alone or in competition with ranitidine, whilst metiamide decreased tyrosinase activity. Lysosomotropic amines had a similar effect to ranitidine, except that induction reached a plateau at 6 h and was insensitive to amiloride. Human melanocytes and pigmented human melanoma cell lines exhibited minimal levels of tyrosinase induction, which was dependent on protein synthesis but not on RNA or DNA synthesis. Constitutive tyrosinase activity in MM96L cells was much less stable than in melanocytes and pigmented melanoma cells. No change was observed in expression of gp75, neural specific octamer binding proteins, or in mRNA levels of tyrosinase, Pmel-17 and gp75 (TRP-1). Tyrosinase was inhibited by the H3 agonist imetit but not by alpha-methylhistamine or the H3 antagonist thioperamide. Overall, this work showed that certain H2 antagonists activate an unstable form of tyrosinase in amelanotic melanoma cells by a post-transcriptional mechanism dependent on protein synthesis. An imidazoline/guanidinium receptor site rather than the H2 receptor appeared to be involved.

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The effect of ranitidine 300 mg po given at 1800 h (famotidine 40 mg/cimetidine 800 mg) on the night time gastric pH was tested using longterm intragastric pH monitoring in 27 patients with and 32 patients without liver cirrhosis. A rise in the gastric pH above 4.0 for more than six hours between 1800 h and 0600 h was considered as sufficient effect (response) of the H2-receptor antagonists on gastric acidity. Among the patients with cirrhosis, there were significantly (p less than 0.005) more non-responders to ranitidine (16 of 27 patients) than in the control group (six of 32). When 13 of the 22 non-responders to ranitidine were subsequently treated with famotidine, only two showed a sufficient rise in their gastric pH. Of the 11 patients not responding to both H2-receptor antagonists, 10 were finally treated with cimetidine and eight did not respond. Plasma levels of all three drugs measured two and four hours after oral administration were not significantly different between cirrhotic and noncirrhotic patients as well as between responders and non-responders. In addition, in all patients plasma levels were far above the corresponding IC50 values. Therefore, differences in the absorption and plasma levels of these drugs cannot account for the frequent non-response in cirrhotics.

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With the exception of diazepam, midazolam, and phenytoin, all of the remaining drugs were chemically compatible with valproate, both in 5% Dextrose Injection, USP(D5W) and in 0.9% Sodium Chloride Injection, USP (Normal Saline -NS). None of the compatible medications produced a significant pH change, discernible gas, particle formation, reduced valproate titer by HPLC analysis (coefficient of variability < 1.5%), or the temporal formation of unidentified UV absorbing (190-400 nm) peaks.

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Thirty-one patients with NUD were randomized to 6 weeks' double-blind alternating treatment with 150 mg ranitidine twice daily or placebo and classified as responders or non-responders.

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Thirteen patients with a faecal weight above 1.5 kg/day (range 1.7-5.7 kg/day and a median small bowel length of 100 cm were studied. Omeprazole 40 mg twice daily or ranitidine 150 mg twice daily were administered for five days in a randomised, double blind, crossover design followed by a three day control period with no treatment. Two patients with a segment of colon in continuation were excluded from analysis which, however, had no influence on the results.

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Aspiration of gastric contents, the most common anaesthetic cause of maternal mortality, is decreased by emptying of the stomach and the use of antacids and H2-receptor antagonists. One hundred and eighty-three mothers presenting for emergency Cesarean section were allocated to three groups. In group 1, the stomach was emptied before operation via an orogastric tube and thereafter 30 ml of sodium citrate 0.3 mol litre-1 was ingested 5-15 min before induction of general anaesthesia (our usual practice). Group 2 received only 30 ml of sodium citrate 0.3 mol litre-1. Group 3 received ranitidine 50 mg i.v. before operation, 5-15 min before induction of anaesthesia, in addition to sodium citrate. Our results show that preoperative gastric emptying with an orogastric tube followed by sodium citrate is preferred if anaesthesia should be induced 15-20 min later. However, the use of ranitidine and sodium citrate is preferred at subsequent times. Although our data show that preoperative gastric emptying decreased the mean intragastric volumes before Caesarean section, the number of patients at risk of acid aspiration was not reduced. In view of these findings and the unpleasantness of orogastric intubation, we suggest that routine preoperative gastric aspiration via an orogastric tube is not justified, although the manoeuvre should still be used following a recent meal.

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This paper describes a method for determining 11 pharmaceuticals in various water sources by SPE followed by LC-(ESI) MS. SPE was carried out with Oasis HLB and the recoveries were 33-67% for 250 and 100 mL sewage water, 55-77% for 500 mL river water and 72-98% for 1 L tap water, with the exception of sulfamethoxazole and omeprazole which showed lower recoveries in all kinds of sample. The LODs in river water were of 5 ng/L for sulfadiazine, trimethoprim, sulfamethazine, sulfamethoxazole, and ranitidine and 10 ng/L for the other compounds. The highest concentrations found in river waters were for sulfamethoxazole (50 ng/L). In influent sewage waters, ranitidine was the most commonly detected compound with a maximum value of 0.24 microg/L.

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Pediatric intensive care unit in a tertiary care children's hospital.

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Of the 569 infants admitted, 53 (9.3%) were treated with ranitidine. Of 74 infants who developed late-onset sepsis, 23 infants received ranitidine and 51 did not. Infants receiving ranitidine were at 7-times greater risk of late-onset sepsis (OR 6.99; 95% CI: 3.78-12.94; P<0.0001). The birth weights and gestational ages of infants with sepsis receiving ranitidine and those not receiving ranitidine were comparable, P=0.59.

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This method permitted correct control of the anesthesia, a quick awakening with a low incidence of nausea and vomiting, a prompt regain of physical and psychological functioning, an early discharge from the hospital, and a larger turnover of patients with lower costs.

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An assessment of the adverse reactions associated with H2-receptor blockers is presented, with particular emphasis towards famotidine. Post-marketing studies on the H2-receptor blockers have shown that they have a low incidence of adverse reactions (1-2% of patients) and are very effective in the treatment of peptic ulcers. The most common adverse reactions are gastro-intestinal, although central nervous system, cardiovascular, haematological, endocrine and hepatic disturbances may occur. Drug interactions and the considerable amount of post-marketing surveillance data, spanning over a decade of use, are also assessed.

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The objective of the present investigation was to prepare and evaluate floating granular delivery system consisting of (i) calcium silicate (CS) as porous carrier; (ii) ranitidine hydrochloride (RH), an anti-ulcer agent; and (iii) hydroxypropyl methylcellulose K4M (HPMC) and ethylcellulose (EC) as matrix forming polymers. The effect of various formulation and process variables on the particle morphology, particle size, micromeritic properties, percent drug content, in vitro floating behavior, and in vitro drug release from the floating granules was studied. The scanning electron microscopy (SEM) of granules revealed that that more pores of CS in secondary coated granules (SCG) were covered by the polymer film than those in primary coated granules (PCG). The formulation demonstrated favorable in vitro floating and drug release characteristics. The in vivo evaluation for the determination of pharmacokinetic parameters was performed in albino rats. Higher plasma concentration was maintained throughout the study period from the floating granules of RH. The enhanced bioavailability and elimination half-life observed in the present study may be due to the floating nature of the dosage form. The results suggested that CS is a useful carrier for the development of floating and sustained release preparations.

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We investigated the effect of ecabet sodium (ecabet) on rat acute esophageal lesions induced by reflux of gastric juice. Ligation of both pylorus and fore-stomach induced the reflux of gastric juice, decreased the amount of mucus and formed hemorrhagic lesions in the esophageal mucosa. Intragastric injection of ecabet reduced the pepsin activity and prevented both the decrease of mucus amount and formation of lesions. Ecabet enhanced the reduction in lesion formation induced by omeprazole and ranitidine without a change in decreased acid concentration and pepsin activity. Digestion of mucosa and the reduction in mucus were prevented by ecabet in the everted HCl and pepsin treated esophageal sac. These results indicate that ecabet prevents esophageal lesions by inhibiting pepsin activity as well as by protecting mucus from degradation. These further implicate the therapeutic potential of ecabet for prevention/treatment of GERD, especially in combination with a proton pump inhibitor or H(2)-antagonist.

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Omeprazole and ranitidine combined with two antibiotics for 1 week are equally effective in the eradication of H. pylori infection, and these results question the role of profound acid suppression in the eradication of the bacterium.

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In this study the incidence and the development of acute renal failure (ARF) in heart transplant recipients is presented. Among the thirteen heart transplant recipients eight of them developed oliguric or nonoliguric ARF. Besides the known factors such as actual condition of the patient, kidney function, peri and post-operative compromised circulation, our results demonstrate the significance of postoperative cyclosporin concentration in combination with the use of other drugs. The results also show the importance of the way cyclosporin has been administrated. The parenteral route of appliance is connected with the greater risk of higher drug concentration in the plasma than the peroral one. In connection with this is the higher incidence of adverse reactions to cyclosporin given parenterally. In addition to ranitidine and captopril, which have been mentioned earlier, the findings of our study indicate that greater attention has to be paid to the treatment with ketoconazol given in combination with cyclosporin, since it results in decreased cyclosporin clearance. Other nephrotoxic drugs like amphotericin also increase the possibility of renal lesions. The incidence of acute renal failure in this group of patients is high. Our data suggest that the reasons for the development of ARF are multifactorial. These data further suggest that a reasonable way to solve nonoliguric form of acute renal failure is to maintain the "internal balance" and that it is not necessary to perform extracorporeal elimination of nitrogen substances, if there are no additional complications (i.e. gastrointestinal bleeding).(ABSTRACT TRUNCATED AT 250 WORDS)

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High-dose once daily oral omeprazole dosing can inhibit acid secretion almost completely but several days elapse before maximum efficacy is established. The acid inhibitory effect obtained with high doses of a histamine H2-receptor antagonist is built up rapidly but has the tendency to fade--the term 'tolerance' has been applied to characterize this phenomenon.

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The higher drug costs for the PPIs are offset by their higher efficacy, making their use cost effective, particularly in severe disease. Efficacy and cost effectiveness are likely to further expand the use of PPIs at the expense of H2RAs as increasing numbers of patients with milder disease are treated.

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One hundred and two patients were entered into a controlled, randomized clinical trial to assess the value of ranitidine versus placebo, given immediately after entry to hospital to modify the outcome of patients admitted to hospital with acute bleeding from peptic ulceration of the stomach or duodenum. The results indicated that ranitidine could not significantly modify the blood requirements, rebleeding rate or operation rate in this patient population during the initial hospital admission.

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Aspiration of gastric contents may contribute to pulmonary complications after thoracotomy. The incidence of gastroesophageal reflux (GER) and tracheal acid aspiration in patients undergoing thoracotomy in the lateral position is unknown. Ranitidine premedication reduces gastric volume, increases gastric pH, and may reduce GER. We used continuous intraluminal esophageal and tracheal pH monitoring probes to investigate the effect of ranitidine on the incidence of GER and tracheal aspiration in 80 adult patients undergoing thoracotomy. The study was placebo-controlled, randomized, and double-blinded. Patients at high risk of GER were excluded from the study. The incidence of acid GER in the placebo and ranitidine groups was 28.2% and 2.5%, respectively (P = 0.006). Multiple episodes of GER occurred in some patients in the placebo group only. The total number of episodes of GER in the placebo and ranitidine groups was 16 and 1, respectively (P = 0.002). The incidence of tracheal acid aspiration in the placebo and ranitidine groups was 7.7% and 2.5%, respectively (not significant). Patients undergoing thoracotomy are therefore at high risk of acid GER, which may lead to tracheal acid aspiration in an appreciable proportion. Premedication with ranitidine significantly reduces, but does not eliminate, the incidence of this potentially life-threatening complication.

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zantac po dosing 2017-11-26

OA improves healing of chronic gastric lesions in rats. The low toxicity and widespread occurrence of OA in plants suggest a potential buy zantac for the development of the triterpene or their derivatives as a new antiulcer drug.

zantac tabs 2015-08-07

Histamine inhibited luminol-dependent chemiluminescence (CL) of granulocytes in a dose-dependent manner, with an ID50 of about 3 X 10(-5) M. Dimaprit, a selective H2-agonist, produced a histamine-like effect. Furthermore, cimetidine, ranitidine, and TZU 0460, which are selective H2-antagonists, but not mepyramine, a selective H1-antagonist, blocked the inhibitory effect of histamine on CL. Thus it may buy zantac be concluded that the inhibitory effect of histamine is mediated via histamine H2-receptors. H1- and H2-antagonists per se, except at extremely high concentrations, had no effect on CL of granulocytes.

child zantac dose 2016-07-22

Name, therapeutic class, and mean daily dose of buy zantac the prescribed drugs.

zantac 150 dosage 2016-02-16

One hundred thirty-six cases with duodenal ulcer bleeding and H. pylori infection (proved by rapid urease test and histology during emergency endoscopy) were studied. One hundred twenty-seven of these patients buy zantac completed a course of triple therapy. In each case, anti-H. pylori IgG titer, gastric biopsies for H. pylori density (score 1 to 5), and evaluation of severity of gastritis were collected at the first endoscopy and 1 month after completion of the triple therapy.

zantac maximum dosage 2015-02-24

Statistically significant differences in the prescription at the 6 centres were only found in two (omeprazole and ranitidine) of the buy zantac 7 active principles. There was wide variety in the prescription of the various brands for all active principles. By assessing the involvement of the pharmaceutical industry in health centres, it was found that the smallest and the most metropolitan centres had different patterns of brand prescription.

zantac dosage pediatric 2015-06-17

Analogues of E-type prostaglandins, such as arbaprostil, enprostil, misoprostol, rioprostil, and trimoprostil, suppress gastric acid secretion and (like native E-type prostaglandins) the chemically modified analogues enhance a number of gastroduodenal mucosal defence factors. These include regulation of the thickness and the composition of the mucous layer at the epithelial surface; modulation of active bicarbonate secretion; hydrophobicity of the surface epithelium; rapid cell proliferation and differentiation after mucosal damage; maintenance of interstitial bicarbonate; and the integrity of the mucosal microcirculation. In theory, this bimodal action makes prostaglandin analogues ideal drugs for treating and preventing lesions of the gastroduodenal mucous membrane. In practice, however, these expectations remain unfulfilled. First, in doses lower than those required to decrease acid secretion, prostaglandin analogues retain cytoprotective properties but are no better than placebo in healing peptic ulcers. Second, in fully antisecretory doses some prostaglandin analogues accelerate ulcer healing compared with placebo and provide healing rates about as high cimetidine, but less than achieved with ranitidine. Third, despite the fact that high doses of some analogues are superior to placebo in alleviating pain associated with ulcer disease, these agents proved inferior to cimetidine and buy zantac ranitidine in relieving pain in most comparative trials. Fourth, enprostil and misoprostol in doses which combine antisecretory with cytoprotective properties perform significantly poorer than ranitidine in preventing relapse of peptic ulcer disease. Fifth, although several uncontrolled observations have suggested a therapeutic benefit of prostaglandin analogues in gastroduodenal haemorrhage, placebo-controlled trials show no effect of arbaprostil in stopping bleeding and in preventing rebleeding.(ABSTRACT TRUNCATED AT 250 WORDS)

zantac 450 mg 2015-04-03

OTC medicines make up an important part of the community pharmacy world. As with most aspects of practice, however, hurdles exist buy zantac that prevent an optimal level of care.

zantac dosing 2015-06-23

Authors describe two cases concerning primary peptic disease: gastric and duodenal ulcer, observed in two children. Clinical pictures, diagnostic and therapeutic methods are described. In this paper we discuss particularly buy zantac new etiopathogenetic and therapeutic factors about peptic disease.

zantac dosage pediatrics 2017-10-16

A series of imidazo[1,2-alpha]pyridinylbenzoxazoles (4) and 5,6,7,8-tetrahydroimidazo[1,2-alpha]pyridinylbenzoxazoles (5) were synthesized and tested for anti-stress ulcer activity in rats. Several compounds were found to be more active than the reference compounds, sucralfate, cimetidine and ranitidine. Some of them exhibited potent protective buy zantac activity against ethanol-induced gastric lesion. The synthesis and structure-activity relationships of these compounds are discussed.

zantac generic 2017-11-30

Although both anti-emetics were associated with a smaller incidence of PONV than was placebo, droperidol was superior to ranitidine in preventing sickness during the immediate postoperative period. The buy zantac need for the "rescue drug" was similar in all groups.

zantac brand name 2016-02-20

The existence of cardiac h1- and h2-receptors is evidenced by pharmacologic studies. Despite of the relatively high content of cardiac histamine it is not clarified whether histamine actually plays a physiologic role - apart from pharmacologic effects - in the regulation of myocardial function and coronary blood flow buy zantac . Under pathophysiologic conditions (during anaphylaxis, surgical procedures, accidents, stress etc.), however, when a local or systemic histamine release occurs both hemodynamic and arrhythmogenic effects are evident. Numerous studies in animal models conclusively demonstrated a role of cardiac histamine as a major mediator of serious arrhythmias. Consequently, a combination of h1- and h2-receptor antagonists (f.e. Dimetinden/Cimetidin) was recommended as a prophylactic treatment against severe anaphylaxis including life-threatening arrhythmias for cardiac patients at risk. There is pharmacologic evidence of both a positive inotropic and chronotropic effect in the human heart via h2-receptor and stimulation of adenylate cyclase. Histamine-induced coronary effects such as vasoconstriction via h1-receptor and coronary dilatation via h2-receptor are not yet sufficiently validated. Studies on the human heart in vitro using coronary strips from explanted hearts and in vivo investigations on the intact coronary system yielded conflicting results. H2-receptor blocking agents cimetidine, ranitidine and famotidine have qualitatively a different pharmocodynamic spectrum of side effects due to differences in chemical structure. Data on cardiac arrhythmias are mostly associated to cimetidine. Symptomatic bradycardia were reported for both ranitidine and cimetidine. A possible negative inotropic effect of famotidine, although presently not validated, requires further studies. Causative and adverse side effects of cimetidine on the cardiovascular system, however, are to be expected extremely seldom due to easily reversible competetive h2-receptor binding. For prophylaxis rapid intravenous injections of h2-blockers, particularly in elder patients with cardiac diseases, should be avoided. Compared to cimetidine, a tendency of explainable difference seems to become apparent for ranitidine and famotidine due to higher receptor affinity.

zantac mg 2015-06-09

The effects of the H1-receptor antagonists promethazine, mepyramine, and chlorpheniramine on ischemic and reperfusion arrhythmias were studied in the isolated perfused rat heart. Promethazine reduced both ischemic and reperfusion arrhythmias (2 x 10(-6)M-7.5 x 10(-6)M). Mepyramine and chlorpheniramine decreased these arrhythmias but at concentrations about 10 times higher. The H2-blockers cimetidine and ranitidine had no antiarrhythmic effect. Promethazine also: (i) increased release of noradrenaline by the heart; and (ii) increased coronary flow in the reperfusion period and in some mildly ischemic zones. It is proposed that promethazine exerts most of its antiarrhythmic effects by a nonspecific mechanism, possibly membrane stabilization; in addition, enhanced buy zantac coronary flow may play a role.

zantac pediatric dose 2017-12-31

103 infants (mean age 3.3 +/- 1.8 mo) with persisting symptoms of reflux despite administration of ranitidine, prescribed previously by a referring physician, at a mean (SD) dose of 9.4 (+/- 3.3) mg/kg/d for at least 2 wk buy zantac (mean 30 d), were submitted to a 24-h pH study and oesophageal biopsy (90/103 patients).

zantac max dose 2016-09-14

The effects of a new H2-receptor antagonist, roxatidine acetate, have been investigated in both clinical and pharmacodynamic trials in Europe and the United States. A series of four double-blind randomized studies are reviewed, reporting the effects of different dose regimens of roxatidine acetate compared with ranitidine and placebo in healthy volunteers using continuous intragastric pH monitoring. These pharmacodynamic studies clearly demonstrate that roxatidine acetate is an effective gastric antisecretory agent, which is up to twice as potent as ranitidine. Brahmi Capsules The results of several clinical studies of roxatidine acetate in patients with gastric as well as duodenal ulcer conducted in Europe, Japan, and the United States are also reviewed. These studies show that roxatidine acetate is comparable to other potent H2-receptor antagonists in terms of cumulative healing rates, pain relief, and safety. Overall, the pharmacodynamic and clinical data indicate that the efficacy of roxatidine acetate 75 mg twice-daily (b.i.d.) does not differ significantly from ranitidine 150 mg b.i.d. Roxatidine acetate is equally effective in the treatment of peptic disease including gastric ulcer, duodenal ulcer, and reflux esophagitis.

zantac overdose 2016-11-04

A multicentre study involving 9 Italian institutions was carried out to compare the efficacy and safety of ranitidine 150 mg b.i.d. and ranitidine 300 mg nocte in the treatment of reflux oesophagitis. 117 patients with histologically proven oesophagitis were randomly allocated to two comparable treatment groups. Efficacy and reliability were evaluated by clinical and laboratory tests at the beginning of the study, and at 3 and 6 weeks; endoscopy and biopsies were performed at the beginning and at 6 weeks. Treatment with ranitidine for 6 weeks led to total disappearance of gastro-oesophageal reflux symptoms in 60% of patients, with percentages of partial improvement varying between 85% and 95% of cases. Improvement in the results of endoscopic examination was 85%, of which 55% were cured. Microscopic examination revealed an improvement of 36% and 44 Effexor Increase Dosage %, with a cure rate of 18% and 26% respectively. With regard neither to the regression of symptoms nor to the macroscopic and microscopic inflammation of the oesophageal mucosa did statistical examination show significant differences in the therapeutic efficacy of ranitidine 150 mg b.i.d. or 300 mg nocte for treatment of reflux oesophagitis.

zantac dosing directions 2015-09-09

Despite histamine being a potent endogenous vasoactive agent released in increasing amounts postburn, its role in postburn oedema formation has been controversial and its effect on burn circulation poorly investigated. The present study investigated the involvement of H(1), H(2) and H(3) receptors in postburn edema in rats exposed to skin and muscle burns and their influence on skin circulation postburn. We used the selective antagonists clemastine (H(1)), ranitidine (H(2)), thioperamide (H(3)) and the selective H(3) receptor agonist, imetit. Results showed that none of the antagonists or the H(3) agonist had significant effect on postburn edema measured by quantitative spectrophotometric analysis of extravasated Evans blue-albumin in the full-thickness burned skin or muscle. Clemastine and thioperamide failed to induce significant effect on blood flow in the partial- or full-thickness skin burn injury as measured by laser Doppler flowmetry, while ranitidine significantly (P<0.01) reduced blood flow in the full-thickness burn. In contrast, the H(3) receptor agonist, imetit, significantly increased blood flow, both in the partial-thickness burn injury (P<0.05) and in the full-thickness burn (P<0.01). Moreover, imetit significantly (P<0.01) increased mean arterial pressure while thioperamide significantly (P<0.01) reduced systemic pressure. In conclusion, H(1), H(2) and H(3) receptors are not important actors in the regulation of vascular patency permeability, whereas H(3) receptors play an important role by increasing skin circulation postburn, presumably by relaxation of vascular Crestor Benefits Reviews smooth muscle and/or by interacting with other inflammatory neurotransmitters. Data also suggest that H(2) receptor blockers may not be best choice for stress ulcer prophylaxis in burn patients.

zantac gerd dosage 2015-02-08

Achieving an objective Cardura Maximum Dose end point reduces stricture recurrence and the need for subsequent dilation. Initial subjective improvement does not predict long-term success.

zantac 150 generic 2015-05-29

Patients were treated with 132 different medication combinations. Mysoline Dosing

zantac generic price 2016-12-21

The application of drug ion-selective electrodes as sensors for the direct determination Paracetamol Tablets of the released drug in a continuous-flow analyzer for automated dissolution studies is described. Flow-through electrodes, selective to chlorpromazine, amitriptyline, propantheline, cimetidine, and ranitidine, have been constructed and used for the dissolution studies of 18 dosage forms using the rotating basket apparatus. The dissolution profiles are obtained in the form of potential peaks versus time.

generic zantac cost 2015-04-26

The percentage of patients with gastric volume >25 mL and pH <2.5 was 5%, 30%, and 0% in groups Botox Online I, II, and III, respectively. Statistically significant difference existed between groups I and II (P = .04) and groups II and III (P = .006). Premedicated morbidly obese and lean patients were comparable (P = .46).

zantac 48 tablets 2015-02-23

Alternating periods of feed deprivation resulted in erosion and ulceration of the gastric squamous epithelial mucosa of each horse. Concurrent treatment with ranitidine resulted in significantly (P < 0.05) less area of ulceration Benicar 75 Mg in the gastric squamous epithelial mucosa. After 7 days' stall confinement, 6 of 7 horses had ulceration in the gastric squamous epithelial mucosa, and 1 horse had a lesion in the glandular mucosa, whereas after 7 days' pasture turnout, 2 horses had reddening of the gastric squamous mucosa along the lesser curvature (P < 0.05).

zantac dosage infants 2016-04-02

A novel method for the quantitative determination of ranitidine hydrochloride (RNH) based on the fluorescence quenching of functionalised CdS quantum dots (QDs) by RNH in aqueous solution was proposed. The method is simple, rapid, specific and highly sensitive with good precision. The thioglycolic acid (TGA)-capped CdS QDs were synthesized from cadmium nitrate and sodium sulfide in alkaline solution. Under the optimal conditions, the Stern-Volmer calibration plot of F(0)/F against concentration of RNH was linear in the range of 0.50-15.0 μg mL(-1) with a correlation coefficient of 0.996. The limit of detection (LOD) was 0.38 μg mL(-1). The method was satisfactorily applied to the direct determination of RNH in pharmaceutical formulations with no significant interference from excipients. The results were found to be in good agreement with those obtained by the reference method and the claimed value. The accuracy and reliability of the method were further ascertained by recovery studies via the standard-addition method, with percentage recoveries in the range of 98.47 to 102.30%. The possible fluorescence quenching mechanism for the reaction was also discussed.

zantac pill 2016-01-18

The pharmacokinetics and pharmacodynamics of ranitidine were studied in 10 hypermetabolic burned patients with normal creatinine clearance and compared with healthy volunteers. Ranitidine was administered as a single 50 mg intravenous bolus and multiple blood samples were obtained up to 10 hours after the dose for determination of plasma ranitidine concentrations. Gastric pH in burned patients was monitored by way of a nasogastric tube. Burned patients exhibited significantly higher (p less than 0.01) ranitidine clearance (mean +/- SD; 10.80 +/- 2.38 versus 7.53 +/- 1.71 ml/min/kg) and steady-state distribution volume (1.63 +/- 0.13 versus 1.16 +/- 0.33 L/kg). Within an hour of administration of drug the gastric pH was greater than or equal to 4.0 in all but one patient. This pH was maintained for at least 6 hours. In five patients the pH was greater than or equal to 4.0 throughout the 10-hour study. Thus, despite increased ranitidine clearance, the recommended dose of ranitidine maintained gastric pH greater than or equal to 4.0 throughout the normal dosing interval in the majority of patients. Dosage adjustment reported for many other drugs after burn injury may not be necessary for ranitidine.

child zantac dosage 2016-08-22

Our results confirm the high prevalence of off-label/unlicensed drug use in the neonatal population and underline a better adherence to indications based on clinical practice, suggesting the need to update information contained in the data sheets of medicines.

zantac 7 tablets 2016-07-31

The possible effects of histamine (HA) locally applied into the preoptic area (POA) on hippocampus-mediated behaviors were studied in adult male rats. Animals were double-implanted unilaterally with microinjection cannulae into POA and hippocampus (HPC). In experiment 1, HA was injected into POA and pyrilamine (H1-HA antagonist) or ranitidine (H2-HA antagonist) were microinjected into the ipsilateral HPC in two different doses. In Experiment 2, HA was injected into POA and the histamine antagonists were microinjected into the contralateral HPC. Ten min later the animals were tested in an automatic monitor activity. Horizontal, ambulatory and vertical movements were measured as general motor exploratory behaviors. Contact time (in seconds) to a circular metal rack positioned in the center of the animal activity monitor was also recorded as goal-directed exploratory activity. Results of Experiment 1 showed that HA in POA exerted an inhibitory influence on general motor behaviors and also on goal-directed activity. Ipsilateral administration of HA-antagonists into HPC blocked the HA effect on behavior. Results of Experiment 2 showed that the administration of the HA-antagonists in any of the two doses used were not able to block the depressive actions on behavior caused by HA into POA. In conclusion, data suggest that POA is linked to the ipsilateral HPC through histaminergic influence to control behavioral patterns induced by novelty.