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Pepsin induced mucosal damage compared to that with cthanol
l9 Helicobacter pylori
Acid secretory and mucosal ulcerogenic responses induced
38 other sections not shown
2M NaCl acid secretion acidification activity administration aged rats agents animals antral arterial aspirin basal basolateral bile buffer capillaries capsaicin CGRP concentrations contact angle cytoprotection decrease dose duodenal bicarbonate secretion duodenal mucosal duodenal ulcer duodenum endogenous epithelial cells epithelium ethanol exposure Figure fluorescence free radicals gastric acid gastric mucosa gastric mucosal blood gastric ulcer gastroduodenal Gastroenterology glands Granger DN HCOj histological hydrophobicity increase indomethacin induced inhibition instillation intestinal intracellular pH intragastric ischemia isolated L-NMMA layer lesions luminal acid luminal pH measured mechanisms mediated mg/kg microvascular mucosal blood flow mucosal damage mucus NaOH nerve neutrophils normal NSAIDs oxygen parietal cells pentagastrin pepsin peptic ulcer peptide perfusion PGE2 Physiol pretreatment prostaglandin proton proton permeability pylori rabbit reduced reperfusion response role saline serosal significantly solution stimulation studies superoxide surface epithelial tissue ulcer disease ulcer healing Upper Gastrointestinal Tract vagal vascular vitro vivo xanthine oxidase