Role of blood flow and alkaline secretion in acid-induced deep duodenal villous injury in rats.
The effect of 16,16-dimethylprostaglandin E2 (dmPGE2) and corticotropin-releasing factor ( CRF) on duodenal blood flow, alkaline secretion, and acid-induced deep duodenal villous injury was studied. The duodena of anesthetized rats were prepared for simultaneous measurement of alkaline secretion by back titration, and blood flow by hydrogen gas clearance; or for perfusion with 0.1 N HCl and histological examination of villous injury. The results revealed that the dmPGE2-induced increase in basal alkaline secretion (due solely to an increase in the volume of secretion) appears to be a better predictor of protection against exogenous acid-induced deep duodenal villous injury than rise in duodenal blood flow, since CRF induces a similar rise in duodenal blood flow but does not enhance alkaline secretion or reduce acid-induced villous damage. The absence of a greater loss of H+ during acid perfusion of the duodenum in the dmPGE2-treated rats, however, suggests that the mechanism of the dmPGE2 protection against acid-induced deep duodenal villous injury cannot be explained entirely by its ability to increase basal duodenal alkaline secretion.[1]References
- Role of blood flow and alkaline secretion in acid-induced deep duodenal villous injury in rats. Leung, F.W. Am. J. Physiol. (1991) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
