Drugs online research references
Aliment Pharmacol Ther. 2002 Apr;16 Suppl 2:107-14.
Wine stimulates gastric acid secretion in isolated rabbit gastric glands via two different pathways.
Matsuno K, Tomita K, Okabe S.
Department of Applied Pharmacology, Kyoto Pharmaceutical University, Japan.
BACKGROUND & AIMS: Alcoholic beverages such as beer and wine are well known to potently stimulate gastric acid secretion, most probably through an increase in circulating gastrin level. The present study examined whether or not wine stimulates gastric acid secretion by a direct effect on parietal cells, enterochromaffin-like (ECL) cells or both. METHODS: Gastric mucosa was isolated from female Japanese white rabbits and gland specimens were prepared by the collagenase digestion method. Acid secretion was assessed by gland accumulation of [14C] aminopyrine. The effects of red wine, ethanol, non-alcoholic wine and drugs were determined by incubating gastric glands with aminopyrine. Radioactivity in solubilized glands was determined by a liquid scintillation counting. RESULTS: Neither wine nor ethanol (diluted 1 : 10(2) to 1 : 10(4)) had any effect on gastric acid secretion, whereas non-alcoholic wine stimulated acid secretion in a dose-dependent manner. All substances, however, significantly stimulated gastric acid secretion in IBMX (phosphodiesterase inhibitor)-pretreated glands. S-0509 (a CCK-2 receptor antagonist) and atropine had no effect on acid secretion stimulated by wine, ethanol or non-alcoholic wine in IBMX-pretreated glands. Famotidine and omeprazole significantly inhibited the acid secretion resulting from all of the above stimulants. BAPTA (an intracellular Ca2+ chelator) inhibited acid secretion stimulated with wine or ethanol in a dose-dependent manner, but did not inhibit secretion stimulated by non-alcoholic wine. CONCLUSIONS: Wine was found to stimulate gastric acid secretion in gastric glands via two pathways, by an ethanol-induced increase in the concentration of intracellular Ca2+ in parietal cells, and by histamine release from ECL cells potentially induced by constituents present in wine.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11966531&dopt=Abstract
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med.uoc.gr
BACKGROUND: Patients who have undergone gastrectomy for benign ulcer do not develop obesity. Furthermore, morbidly obese patients who undergo biliopancreatic diversion (BPD), Roux-en-Y gastric bypass (RYGBP) and vertical banded gastroplasty (VBG) plus truncal vagotomy, may lose more weight compared with patients who undergo VBG alone. A common characteristic of the above is the reduction of gastric hydrochloric acid secretion. We investigated whether reduction in gastric acid increases dietary-induced thermogenesis because of maldigestion of foods, and this may account for the greater weight loss in the above situations. MATERIALS AND METHODS: 22 volunteers without symptoms from the upper gastrointestinal tract were studied. Gastric pH was measured and resting energy expenditure (MREE), using indirect calorimetry, was determined before and 8 hours after consumption of a standard meal. Parameters were measured again after 2 months administration of proton pump inhibitors in all volunteers. RESULTS: Although significant reduction of gastric acid secretion occurred (p < 0.01), following administration of proton pump inhibitors, the fasting and postprandial MREE remained unchanged (p > 0.05). CONCLUSIONS: The reduction in gastric acid secretion does not increase the energy requirements for digestion of foods and thus is neither the mechanism responsible for the increased weight loss observed after RYGBP or BPD, nor the explanation for the lean appearance of gastrectomized patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11975219&dopt=Abstract
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Am J Surg. 2002 Apr;183(4):441-4.
Effect of hypergastrinemia on pancreatic carcinogenesis.
McDonald JM, Longnecker DS, Bell RH Jr.
Department of Surgery, Veterans Affairs Puget Sound Health Care System and the University of Washington School of Medicine, Seattle, WA 98108, USA.
BACKGROUND: Previous studies in our laboratory demonstrated that pancreatic carcinomas in rodents express receptors for the peptide hormone gastrin that are not present in normal adult pancreas. In view of an abundant literature suggesting that gastrin may promote growth of various gastrointestinal tissues and tumors, the effect of hypergastrinemia on the process of pancreatic carcinogenesis was evaluated. METHODS: Rats received subcutaneous injections of the pancreatic carcinogen azaserine at 19 and 26 days of age. Starting at 12 months of age, animals were randomized to treatment with the proton pump inhibitor lansoprazole or vehicle by gavage for 6 months. At autopsy, pancreatic wet weight normalized to body weight was recorded, as well as the number of benign and malignant pancreatic lesions. RESULTS: Serum gastrin levels were determined by radioimmunoassay and showed a greater than two-fold increase in lansoprazole-treated animals. Pancreatic wet weight in hypergastrinemic rats was increased compared to controls (p <0.05). Premalignant lesions such as acidophilic atypical acinar cell foci, adenomas, heterogeneous phenotypic populations of nodules within nodules, and carcinoma-in-situ were not increased in the hypergastrinemic group. Likewise, there was no difference in the incidence of invasive carcinoma in hypergastrinemic animals (10%) compared to controls (5.7%). CONCLUSION: Hypergastrinemia stimulated an increase in pancreatic weight, but did not stimulate development of premalignant lesions or progression to cancer in the azaserine model of rat pancreatic acinar cell carcinoma.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11975934&dopt=Abstract
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