Drugs online research references
J Am Vet Med Assoc. 2003 Aug 1;223(3):336-9.
Odds of moderate or severe gastric ulceration in racehorses receiving antiulcer medications.
Orsini JA, Haddock M, Stine L, Sullivan EK, Rabuffo TS, Smith G.
New Bolton Center, School of Veterinary Medicine, University of Pennsylvania, Kennett Square, PA 19348, USA.
OBJECTIVE: To determine the odds of moderate or severe gastric ulceration in racehorses treated with various antiulcer medications. DESIGN: Unmatched case-control study. ANIMALS: 798 horses in active race training (252 Thoroughbreds and 546 Standardbreds). Only horses that had been receiving a single antiulcer medication or no antiulcer medication for at least 2 weeks prior to examination were included. PROCEDURE: Gastroscopy was performed on each horse by a single individual who was not aware of the horses' antiulcer treatments, and severity of gastric ulceration was scored. Signalment and medication history were recorded. Logistic regression was used to determine whether identification of moderate or severe ulceration was associated with treatment, age, breed, or sex. Treatments were grouped as no treatment, buffer, sucralfate, histamine type 2 receptor antagonist, compounded omeprazole, proprietary omeprazole at a low dosage, and proprietary omeprazole at a high dosage. RESULTS: Only proprietary omeprazole was associated with significantly lower odds of moderate or severe ulceration, compared with no treatment. Risks of moderate or severe gastric ulceration in horses receiving a buffer, sucralfate, a histamine type 2 receptor antagonist, or compounded omeprazole were not significantly different from risks in horses receiving no antiulcer medication. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that the proprietary formulation of omeprazole was associated with a significantly lower risk of moderate or severe gastric ulceration, compared with no treatment, in racehorses in active race training, whereas other antiulcer medications were not.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12906229&dopt=Abstract
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Am J Physiol Gastrointest Liver Physiol. 2003 Dec;285(6):G1242-8. Epub 2003 Aug 07.
Demonstration of a functional apical sodium hydrogen exchanger in isolated rat gastric glands.
Kirchhoff P, Wagner CA, Gaetzschmann F, Radebold K, Geibel JP.
Department of Surgery, Yale University School of Medicine, New Haven, Connecticut 06511, USA.
Previous studies have shown that gastric glands express at least sodium-hydrogen exchanger (NHE) isoforms 1-4. Our aim was to study NHE-3 localization in rat parietal cells and to investigate the functional activity of an apical membrane NHE-3 isoform in parietal cells of rats. Western blot analysis and immunohistochemistry showed expression of NHE-3 in rat stomach colocalizing the protein in parietal cells together with the beta-subunit of the H(+)-K(+)-ATPase. Functional studies in luminally perfused gastric glands demonstrated the presence of an apical NHE isoform sensitive to low concentrations of 5-ethylisopropyl amiloride (EIPA). Intracellular pH measurements in parietal cells conducted in omeprazole-pretreated superfused gastric glands showed an Na+-dependent proton extrusion pathway that was inhibited both by low concentrations of EIPA and by the NHE-3 specific inhibitor S3226. This pathway for proton extrusion had a higher activity in resting glands and was inhibited on stimulation of histamine-induced H(+)-K(+)-ATPase proton extrusion. We conclude that the NHE-3 isoform located on the apical membrane of parietal cells offers an additional pathway for proton secretion under resting conditions. Furthermore, the gastric NHE-3 appears to work under resting conditions and inactivates during periods of H(+)-K(+)-ATPase activity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12907430&dopt=Abstract
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Vestn Khir Im I I Grek. 2003;162(3):97-100.
[Pharmacotherapy in complex treatment of ulcerous stenosis]
[Article in Russian]
Rukhliada NV, Nazarov VE, Ermolaev IA.
The authors present results of the examination and treatment of 64 patients with ulcer disease complicated by stenosis (27 patients had compensated stenosis, 33--subcompensated and 4 patients--decompensated stenosis). The investigation of the dynamics of main pathophysiological disorders and specific action of medicinal preparations has revealed the causes of ineffectiveness of standard antiulcerous therapy. The principles of conservative treatment of ulcer disease with stenosis are developed. The proposed method of treatment resulted in cicatrization of the ulcer, disappearance of the inflammatory edema of the mucosa, reestablishment of patency of the pyloro-duodenal canal and stable remission of the disease in 58 patients (followed up during the period from 6 months till 3 years). Only 6 (9.4%) out of 64 patients were operated upon (2--with decompensated and 4 with subcompensated stenosis). The results obtained show that it is necessary to determine the indications to operations in patients with ulcerous stenosis after complex conservative therapy and the reassessment of the degree of evacuatory disorders.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12942622&dopt=Abstract
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