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A mechanism for prostaglandin cytoprotection

โœ Scribed by James M. McGreevy; Frank G. Moody


Book ID
101738404
Publisher
John Wiley and Sons
Year
1980
Tongue
English
Weight
392 KB
Volume
67
Category
Article
ISSN
0007-1323

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โœฆ Synopsis


Abstract

Topical 16,16-dimethyl (dm) prostaglandin E2 produces an alkaline secretion from the canine stomach. This study attempts to assess whether this prostaglandin-induced secretion might have a cytoprotective role. Chambered ex vivo perfused wedges of canine stomach were divided into equal halves: a control and test side. The mucosa of each half was sequentially exposed to isosmotic hydrochloric acid, 20ฮผg, of 16,16 dm PGE2 in acid, 20 mmol aspirin + 20 ฮผg of dm PGE2 in acid then isosmotic acid. The test side received 40 mmHg pneumatic counterpressure to reduce the prostaglandin-induced fluid movement before, during and after the aspirin exposure. The mucosal lesions produced on each side were graded 0 to 4. If prostaglandin exerts its cytoprotective effect by stimulating an alkaline secretion, elimination of that secretion with counterpressure should prevent a cytoprotective action. Nine dogs were studied.

Topical prostaglandin increased transmucosal fluid movement from 10 ฮผl/min to 65 ฮผl/min. Counterpressure decreased this volume flow by 50 per cent (P < 0ยท01); it also decreased mucosal blood flow on the test side by 20 per cent (P < 0ยท05). The lesions on the counterpressure side were worse 2ยท0ยท0ยท6 v. 0ยท8 ยฑ 0ยท3 (P < 0ยท01). Thus the greater damage in the counterpressure group could have been caused by diminished fluid movement or by reduced blood flow or a combination of both factors. Although this study cannot distinguish between these possibilities, it seems likely that the prostaglandin-induced alkaline secretion has a cytoprotective role.


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