Product Description

Indications and Usage:

Acid peptic disease both active disease treatment and for maintenance therapy. Gastroesophageal reflux disease and erosive esophagitis. Hypersecretory states like Z.E. syndrome etc.

Mechanism of Actions:

Domperidone is a peripheral D2-receptor antagonist, which regulates the motility of gastric and small intestinal smooth muscle. It increases the duration of antral and duodenal contractions and also LES resting pressure, thus stimulating gastric emptying and is also effective in relief of symptoms of reflux esophagitis. Antiemetic activity is due to the blockade of receptors in the chemoreceptor trigger zone. Esmoprazole inhibits the secretion of gastric acid by irreversibly blocking the enzyme system of H+/K+ ATPase of the gastric parietal cell. It is activated at an acidic pH to a sulphenamide derivative that binds irreversibly to H+/K+ ATPase, an enzyme system found at the secretory surface of parietal cells. It thereby inhibits the final transport of hydrogen ions (via exchange with K ions) into the gastric lumen.

Drug Interactions:

Esesmoprazole may have fewer drug interactions than esmoprazole. The absorption of certain drugs may be affected by stomach acidity. Therefore, esmoprazole and other PPIs that reduce stomach acid also reduce the absorption and concentration in blood of ketoconazole and increase the absorption and concentration in blood of digoxin. This may lead to reduced effectiveness of ketoconazole or increased digoxin toxicity, respectively

Pharmacology:

Domperidone blocks the action. It has strong affinities for the D2 and D3 receptors, which are found in the chemoreceptor trigger zone, located just outside the blood brain barrier, which, among others, regulates nausea and vomiting (area postrema on the floor of the fourth ventricle and rhomboid fossa). Esmoprazole is a Proton pump inhibitors which block acid at the final common pathway of secretion-that is, at the proton pump-regardless of the stimulus of acid secretion, and thereby offer by far the most potent suppression of gastric acid.