| Autor: |
Mersereau, W. A., Lough, J. O., Hinchey, E. J. |
| Zdroj: |
Digestive Diseases and Sciences; November 1988, Vol. 33 Issue: 11 p1445-1453, 9p |
| Abstrakt: |
The etiology of the deep bandlike necrotic gastric mucosal lesions induced by the oral administration of corrosive agents in the rat is unclear. An understanding of why the lesions are so precisely localized and how they develop should increase our understanding of the mechanisms by which the prostaglandins prevent them. This study utilizes an innocuous dye to demonstrate that the initial mucosal contact by orally administered agents is restricted to the crests of mucosal folds. A sequential study of lesion development at the fold crest indicates that coagulative necrosis occurs on contact and that the vascular defects, hemorrhage and congestion, are secondary to deep corrosion injury. Exogenous prostaglandin and 0.35 N HCl were found to abolish mucosal folding and hence prevent the fold-related lesions. Inhibition of prostaglandin synthesis was found to sensitize the mucosal fold crest to injury by 0.35 N HCl, and hence the use of indomethacin as a proof that endogenous prostaglandin synthesis plays a role in preventing bandlike lesions by such agents is questioned. It is concluded that the gastric mucosal fold plays a major role in localizing mucosal injury to parallel bands and that the obliteration of these sensitive sites may explain the protective effect of an ever-expanding number of agents. As lesion genesis appears to be the result of a contact artifact, the use of this model in the study of the physiological role played by gastric prostaglandins is seriously questioned. |
| Databáze: |
Supplemental Index |
| Externí odkaz: |
|
Full text from SpringerLink