1995
DOI: 10.1248/bpb.18.223
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Effect of a Combination of Ecabet Sodium and Cimetidine on Experimentally Induced Gastric Lesions and Gastric Mucosal Resistance to Ulcerogenic Agents in Rats.

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Cited by 47 publications
(43 citation statements)
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“…19) The formation of gastric mucosal lesions by necrotizing agents such as HCl and EtOH has been reported to involve the depression of these gastric defensive mechanisms. 20) HCl-EtOH-induced gastric ulcers also promote stasis in gastric blood flow which contributes to the development of the hemorrhagic and necrotic aspects of tissue injury. 2) It has been found that EtOH-induced ulcers are not inhibited by antisecretory agents such as cimetidine, but are inhibited by agents that enhance mucosal defensive factors such as prostaglandins.…”
Section: Resultsmentioning
confidence: 99%
“…19) The formation of gastric mucosal lesions by necrotizing agents such as HCl and EtOH has been reported to involve the depression of these gastric defensive mechanisms. 20) HCl-EtOH-induced gastric ulcers also promote stasis in gastric blood flow which contributes to the development of the hemorrhagic and necrotic aspects of tissue injury. 2) It has been found that EtOH-induced ulcers are not inhibited by antisecretory agents such as cimetidine, but are inhibited by agents that enhance mucosal defensive factors such as prostaglandins.…”
Section: Resultsmentioning
confidence: 99%
“…The ability of gastric mucosa to resist injury by endogenous secretions (acid, pepsin and bile) and ingested irritants (e.g., alcohol), can be attributed to a number of factors that have been referred to collectively as mucosal defense [28] . Gastric mucosal lesions induced by necrotizing agents such as ethanol and strong alkalis are due to depression of the gastric defensive mechanisms [29] . Although ethanol-induced ulcers are not inhibited by anti-secretory agents such as cimetidine, they are inhibited by agents that enhance mucosal defensive factors such as prostoglandins [30] .…”
Section: Discussionmentioning
confidence: 99%
“…Gastric ulcer seems to be generated from over-secretion of gastric juice and imbalance of defensive and aggressive factors involved in maintaining gastric mucosal integrity (McQuaid and Isenberg, 1992). The formation of gastric mucosal lesions by necrotizing agents such as HCl and ethanol has been shown to be associated with depression of gastric defensive mechanisms (Kinoshita et al, 1995). Therefore, acid production regulators such as proton pump inhibitors widely used in clinic (Pisegna, 2002), appear to accelerate the healing of gastric ulcers and gastritis by potent and longlasting antisecretory actions (Welage, 2003).…”
Section: Effect Of Mb Extract-components On the Gastric Secretionmentioning
confidence: 99%