1981
DOI: 10.1016/0016-5085(81)90182-7
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Role of prostaglandins in the formation of aspirin-induced gastric ulcers

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Cited by 197 publications
(44 citation statements)
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“…In most cases, the reduction of gastric blood flow by itself is not sufficient to produce gastric lesions but it renders the mucosa more susceptible to damage induced by stress, ischemia-reperfusion, corrosive substances (ethanol, 25% NaCl, bile salts) and topically active compounds (ASA) [13]. By blocking the activity of COX-1 by NSAIDs in intact or inflamed gastric tissue, an increase in the gastric acid was observed suggesting that gastric acid plays an important role in the NSAID-induced gastropathy [10,25]. This enhancement in gastric secretion induced by NSAIDs might be more complicated issue, since classic NSAID, indomethacin increased basal but not pentagastrin-stimulated acid secretion in humans while in rats it was capable of increasing both basal-and secretagogue-stimulated gastric acid secretion mainly in inflamed tissue [26,27].…”
Section: Historical and Epidemiological Impact Of Nonsteroidal Anti-imentioning
confidence: 96%
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“…In most cases, the reduction of gastric blood flow by itself is not sufficient to produce gastric lesions but it renders the mucosa more susceptible to damage induced by stress, ischemia-reperfusion, corrosive substances (ethanol, 25% NaCl, bile salts) and topically active compounds (ASA) [13]. By blocking the activity of COX-1 by NSAIDs in intact or inflamed gastric tissue, an increase in the gastric acid was observed suggesting that gastric acid plays an important role in the NSAID-induced gastropathy [10,25]. This enhancement in gastric secretion induced by NSAIDs might be more complicated issue, since classic NSAID, indomethacin increased basal but not pentagastrin-stimulated acid secretion in humans while in rats it was capable of increasing both basal-and secretagogue-stimulated gastric acid secretion mainly in inflamed tissue [26,27].…”
Section: Historical and Epidemiological Impact Of Nonsteroidal Anti-imentioning
confidence: 96%
“…Epithelial cells is known to trap of charged NSAIDs resulting in enhanced apoptosis subsequent to uncoupling of oxidative phosphorylation. In addition particular lines of gastric defense system including two major ones, namely, mucus and bicarbonate secretion and gastric mucosal blood flow are markedly inhibited [10,13]. This results in decreasing the effectiveness of juxtamucosal pH gradient in protecting gastric epithelium and limits the blood flow to the organ such as stomach rendering it more vulnerable to the damaging action of gastric acid [14].…”
Section: Historical and Epidemiological Impact Of Nonsteroidal Anti-imentioning
confidence: 97%
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