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368 bytes added ,  15:38, 28 January 2009
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Gastro-intestinal prostaglandins (for example, PGI2 and PGE2) normally have a protective influence over the gastric mucosa, by inhibiting the secretion of gastric acid and promoting that of mucus. NSAID inhibition of COX-1 function leads to the reduced synthesis of these prostaglandins, causing '''ulceration of the gastro-intestinal tract'''. Lesions of the large intestine have also been demonstrated following the use of phenylbutazone in the horse. Although NSAIDs are normally absorbed in the stomach, phenylbutazone may bind to feed and become released in this more distal area of the tract resulting in ulceration.
 
Gastro-intestinal prostaglandins (for example, PGI2 and PGE2) normally have a protective influence over the gastric mucosa, by inhibiting the secretion of gastric acid and promoting that of mucus. NSAID inhibition of COX-1 function leads to the reduced synthesis of these prostaglandins, causing '''ulceration of the gastro-intestinal tract'''. Lesions of the large intestine have also been demonstrated following the use of phenylbutazone in the horse. Although NSAIDs are normally absorbed in the stomach, phenylbutazone may bind to feed and become released in this more distal area of the tract resulting in ulceration.
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Prostaglandins also have a vasodilatory action, and so local production in the kidney is important for maintaining normal renal perfusion. NSAID interference will therefore lower renal blood flow, giving rise to '''nephrotoxicity''', and so use in renal patients must be carefully considered. Care must also be taken when administering these drugs peri-operatively.
    
==Drugs in This Group==
 
==Drugs in This Group==
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