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Oral or intravenous administration of ranitidine inhibits both basal gastric secretions and gastric acid secretion induced by histamine, pentagastrin and other secretagogues. On a weight basis ranitidine is between 4 and 9 times more potent than cimetidine. After oral administration of ranitidine, the plasma concentrations of ranitidine achieved are directly related to the dose administered. Pepsin secretion is MS-Contin (Morphine Sulfate Controlled-Release)- Multum inhibited by ranitidine, but secretion of gastric mucus is not affected.

Ranitidine does not alter the elective of bicarbonate or enzymes from the pancreas in response to secretin and pancreozymin. Reduction in gastric acid secretion induced by ranitidine 150 mg twice daily for 7 days did not cause bacterial overgrowth in the stomach.

Pulse rate, blood pressure, electrocardiogram and electroencephalogram were not significantly affected in man following recommended doses of ranitidine. One study in 30 male duodenal ulcer patients showed a significant decrease in basal thyroxine levels after 4 weeks' treatment with 300 mg ranitidine daily, but no significant change in thyroid stimulating hormone was noted.

Acute administration of 50 mg ranitidine intravenously had no effect on plasma aldosterone in healthy male volunteers whereas it caused a significant reduction in vasopressin. Cimetidine 200 mg intravenously had a similar effect on vasopressin.

No umckaloabo trial data available. Peak plasma levels occur about 2-3 hours after oral administration of ranitidine. Absorption is not significantly altered by food or concurrent antacid administration.

Two distinct peaks or a plateau in the absorption phase suggest reabsorption of drug secreted into the intestine. The elimination half-life is approximately 2 hours. Plasma concentrations decline biexponentially, with a terminal half-life of 2 to 3 hours. The major route of elimination of unchanged ranitidine is renal. Patients over 50 years of age.

Short-term treatment of proven duodenal ulcer and gastric ulcer, including intravenous use for prophylaxis against recurrent haemorrhage. Maintenance treatment to reduce the risk of relapse in duodenal ulcer.

Maintenance treatment for periods up to one year to reduce the risk of relapse in patients with documented healing of benign gastric ulcer.

Treatment of gastrinoma (Zollinger-Ellison syndrome). Short-term symptomatic MS-Contin (Morphine Sulfate Controlled-Release)- Multum of reflux oesophagitis unresponsive to conservative antireflux measures and simple drug therapies such as antacids.

Maintenance treatment to reduce the risk of relapse of reflux oesophagitis. Treatment of scleroderma oesophagitis. The intravenous injection is indicated where oral treatment is inappropriate. Treatment with a histamine H2-antagonist may mask symptoms associated with carcinoma of the stomach and, therefore, may delay diagnosis of the condition.

Accordingly, where gastric ulcer is suspected, the possibility of malignancy should be excluded Quadramet (Samarium SM 153 Lexidronam)- FDA therapy with Zantac oral liquid, tablets or injection is instituted.

The risk of MS-Contin (Morphine Sulfate Controlled-Release)- Multum recurrence is determined by many MS-Contin (Morphine Sulfate Controlled-Release)- Multum. Evidence from controlled clinical trials of up many people understand the importance of healthy eating 18 months continuous treatment with Zantac has not revealed any undue untoward effects.

In association with rapid administration of Zantac injection, has been reported rarely, case in patients with factors predisposing to cardiac rhythm disturbances. Recommended rates of administration MS-Contin (Morphine Sulfate Controlled-Release)- Multum not be exceeded. The MS-Contin (Morphine Sulfate Controlled-Release)- Multum of higher than recommended doses of intravenous H2-antagonists has been associated with rises in liver enzymes when treatment has been extended beyond five days.



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