Omeprazole Sodium for Injection
Omeprazole is a racemic mixture of two active optical enantiomers. It can reduce the secretion of gastric acid through a highly targeted mechanism. It is a special inhibitor of acid pump in gastric parietal cells. The effect of this product is rapid, once a day dose can reversibly inhibit the secretion of gastric acid.
Omeprazole is a kind of weak basic substance, which is concentrated and converted into active substance in the highly acidic environment of inner tubule of gastric parietal cells, which inhibits H +, K + - ATPase (proton pump). The inhibitory effect on the final step of gastric acid formation was dose-dependent, and highly inhibited basal and irritant gastric acid secretion, but not related to stimulants.
Omeprazole was given intravenously to human body, which inhibited gastric acid secretion in a dose-dependent manner. In order to achieve the same effect of reducing gastric acidity as repeated oral administration of 20 mg omeprazole, 40 mg omeprazole was recommended for the first time. Intravenous injection of 40 mg omeprazole rapidly reduced gastric acidity, with an average decrease of 90% within 24 hours. The inhibitory effect of omeprazole on gastric acid secretion was related to the area under the drug time curve (AUC), but not to the blood concentration at the time of administration.
Helicobacter pylori is associated with acid peptic diseases, including duodenal ulcer and gastric ulcer. Helicobacter pylori infection is associated with 95% and 70% of duodenal ulcer and gastric ulcer respectively. Helicobacter pylori is the main cause of gastritis. Helicobacter pylori, together with gastric acid, is a major cause of peptic ulcer.
Omeprazole combined with antibiotics can eradicate Helicobacter pylori, which is associated with rapid relief of symptoms, high rate of gastric mucosal repair and long-term remission of peptic ulcer disease, thus reducing complications such as gastrointestinal bleeding, and reducing the need for long-term use of antacids.
Any method, including proton pump inhibitor induced decrease of gastric acid, will increase the number of normal flora in the gastrointestinal tract. The risk of Salmonella and Campylobacter infection may be slightly increased when treated with anti acid drugs.
In the study of long-term administration of omeprazole in rats, enlargement of ECL cells and benign tumor in the stomach were observed, which was the result of gastric acid inhibition due to persistent hypergastrinemia. Similar findings were found after treatment with H2 receptor antagonists and proton pump inhibitors and after partial base resection. Obviously, these changes are not the direct effect of the above drugs.
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