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Titlebook: Side-Effects of Anti-Inflammatory Drugs; Part Two Studies in K. D. Rainsford,G. P. Velo Book 1987 MTP Press Limited 1987 Arthritis.Glucoco

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Al(OH)3 inhibits aspirin-induced gastric lesions in cats with Heidenhain pouchicularly Al(OH)., also induce release of PGE. into submucosa. Therefore the effect of A1(OH). added to the main stomach was studied on gastric erosions induced by instillation of acetylsalicylic acid (ASA) in the pouch.
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Prostaglandins prevent red streaks in rat gastric mucosa caused by intravenous aspirin but not by sad rats had intragastric instillation of 0.15 M HC1. ASA or SA, 150 mg/kg or saline, was given i.v. as a bolus. After 180 min drug exposure, stomachs were examined after in situ fixation and lesion area assessed by planimetry.
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Mechanisms of gastric contrasted with intestinal damage by non-steroidal anti-inflammatory drugsgastro intestinal (GI) tract. Some drugs such as aspirin and other salicylates cause damage principally in the stomach and duodenum.. However, there is now increasing evidence from clinical reports in man that some other NSAIDs may, in addition to causing damage in these upper GI regions., also caus
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Limitations of laboratory models in predicting gastrointestinal toleration of oxicams and other antition of the structural and physical constraints placed upon those compounds believed to be potential NSAIDs and to the role played by pharmacokinetic properties in delivery of drug to the site of inflammation and the maintenance there of effective drug concentrations. The evolution of such appreciat
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Early and late phases in the formation by anti-inflammatory drugs of intestinal lesions in ratsost attention has been devoted to the stomach, mainly because in humans the incidence of these reactions in the stomach is much greater than in the intestine. Apart from some sporadic cases there were almost no reports of intestinal toxicity of NSAIDs in humans during these years, and the attention
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