Drugs online research references
Nippon Yakurigaku Zasshi. 1988 Jul;92(1):39-47.
[Effect of an H+, K+-ATPase inhibitor, omeprazole (OPZ), on gastric acid secretion and gastric or duodenal lesion. Comparison with an H2-receptor antagonist, famotidine (FMD)]
[Article in Japanese]
Haga K, Asano K, Osuga K, Maruyama Y.
Research Laboratories, Yoshitomi Pharmaceutical Industries, Ltd., Fukuoka, Japan.
In pylorus ligated rats, OPZ inhibited gastric acid secretion dose-dependently, with a potency greater than that of FMD. At the same time, OPZ increased gastric K+ secretion and inhibited pepsin and Na+ secretions at the highest dose. In Heidenhain pouch dogs, single injection of OPZ inhibited gastric acid secretion induced by histamine to a degree almost equal to that by FMD. In the case of repeated administration, anti-secretory activity of OPZ was enhanced by up to several days and then remained constant. After several days, the inhibitory activity of OPZ was more potent and longer than that of FMD, and it still had not ceased 22hr after administration. In pylorus ligated rats, OPZ prevented gastric ulceration, and the potency was greater than that of FMD. OPZ promoted healing of gastric and duodenal ulcers induced by acetic acid in rats. At the same doses, FMD failed to promote the healing of both ulcers. In water-immersion stressed rats, OPZ prevented formation of gastric erosions, with a potency greater than that of FMD. In addition, OPZ prevented formation of gastric erosions induced by ethanol in rats. These results indicate that the anti-secretory and anti-ulcer activities of OPZ are superior to those of FMD, so that OPZ should have excellent therapeutic application for peptic ulcers.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2906028&dopt=Abstract
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Digestion. 1986;35 Suppl 1:70-83.
Gastric regulatory peptides in rats with reduced acid secretion.
Bishop AE, Allen JM, Daly MJ, Larsson H, Carlsson E, Bloom SR, Polak JM.
Gastric acid secretion is known to be controlled by a complex system of interacting factors. Amongst these, regulatory peptides make a significant contribution. In the present study, immunocytochemistry and radioimmunoassay were used to investigate gastric regulatory peptides in animals with pharmacologically reduced gastric acid secretion. Increased numbers of densely immunostained antral gastrin-immunoreactive (G) cells were seen in rats which had been rendered virtually achlorhydric by administration of high-dose (400 mumol/kg daily) omeprazole over a 10-week period. These morphological changes were accompanied by increases in the plasma, antral and fundic concentrations of gastrin, as measured by radioimmunoassay. In contrast, antral somatostatin-containing cells were reduced, and there was a corresponding fall in the tissue content of the peptide. Ten weeks after treatment had ceased, the peptide profiles had returned to normal. No other regulatory peptide, whether endocrine or neural, appeared to alter during treatment with high-dose omeprazole. Treatment with high-dose (700 mumol/kg daily) ranitidine also caused an elevation in the G cell population and the antral and plasma content of gastrin, but to a lesser extent than that observed during omeprazole treatment. Somatostatin cells and tissue levels did not alter in these animals, and no other morphological changes could be detected. Radioimmunoassay, however, measured reduced quantities of vasoactive intestinal peptide, peptide histidine isoleucine and calcitonin gene-related peptide. Achlorhydria, induced by omeprazole at a dosage of 250-500 times that required for effective acid inhibition in man and animals, therefore resulted in reciprocal changes in gastrin and somatostatin cells. These changes are support for the postulated roles of these peptides in the control of gastric acid secretion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3792673&dopt=Abstract
note: kwd match prilosec online literature
Peptides. 1985 Jan-Feb;6(1):153-6.
Gastric erosions induced by intracisternal thyrotropin-releasing hormone (TRH) in rats.
Goto Y, Tache Y.
Intracisternal injection of TRH (1 microgram) under light ether anesthesia induced within 4 hr gastric lesions in 24-hr fasted rats maintained unrestrained at room temperature. Saline, ovine corticotropin-releasing factor (oCRF, 10 micrograms), or human pancreatic growth hormone-releasing factor [hpGRF(1-40), 10 micrograms] tested under the same conditions did not modify the integrity of the gastric mucosa. TRH injected intravenously (100 micrograms/kg) proved to be ineffective. The production of gastric erosions elicited by intracisternal TRH (0.1-1 microgram) or by a stabilized TRH analog, RX 77368 [pGlu-His-(3,3'-dimethyl)-ProNH2, (0.01-0.1 microgram)] was dose-dependent. RX 77368 shows an enhanced potency over TRH. TRH action on gastric mucosa was reversed by atropine, omeprazole and cimetidine. These results demonstrate that TRH, unlike the other hypothalamic releasing factors CRF or GRF, is able to act within the brain to cause the formation of gastric erosions probably through mechanisms involving changes in gastric acid secretion. Intracisternal injection of TRH or its potent analog RX 77368 appears also as a new, simple method to produce centrally mediated experimental gastric erosions in 24 hr-fasted rats.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3921944&dopt=Abstract
note: kwd match prilosec online literature
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