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OMEPRAZOLE is a substituted benzimidazole that functions to decrease gastric acid secretion through irreversible binding and inhibition of the H+K+ATPase enzyme located within the secretory canaliculi of the gastric parietal cells (Pilbrant and Cederberg 1985, Regårdh and others 1985). Inhibition of gastric acid secretion and maintenance of a gastric fluid pH above 4.0 is critical in the treatment and prevention of gastro-oesophageal reflux disease (GERD) in human beings (Bell and others 1992). Ulcer disease of the non-glandular stomach in horses (equine gastric ulcer syndrome) has been compared to GERD, and like the condition in human beings, objectives of treatment centre around suppression of acid secretion and increasing gastric fluid pH. Studies in both human beings and horses have shown that orally administered omeprazole is highly effective in increasing gastric fluid pH, therefore making it one of the more common medications used for the treatment of these conditions (Bell and others 1992, MacAllister 1999, Buchanan and Andrews 2003, Bell and others 2007).
In human beings, the bioavailability of omeprazole following oral administration is relatively low (approximately 40 per cent), due to the drug's instability in acidic gastric fluid and the fact that it undergoes hepatic first-pass metabolism (Regårdh and others 1985). Special formulations using capsules containing enteric-coated, acid-resistant granules have allowed improved systemic bioavailability in human beings by preventing acidic degradation of omeprazole in the stomach (Pilbrant and Cederberg 1985). Still, this limit in the bioavailability of the oral formulation has prompted studies investigating the alternative of rectal administration in several species, including human beings, rabbits and rats (Sastry and others 1993, Choi and others 1996). When administered rectally, omeprazole is able to avoid preabsorptive degradation in the stomach as well as partially avoid first-pass metabolism (Choi and others 1996). …
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