Studies on the oxygen radical mechanism involved in the small intestinal reperfusion damage.
Characteristic mucosal lesions develop in the small intestine during ischaemia and hypotension. This tissue damage can be further aggravated in the immediate reperfusion phase, presumably secondary to the generation of oxygen free radicals which have been proposed to be generated in this situation through the hypoxanthine-xanthine oxidase system. This was further investigated in the cat small intestine using a standardized regional intestinal hypotension model in which the effects of allopurinol (a xanthine oxidase inhibitor) were compared to those of an exogenous supply of inosine. The grade of mucosal damage, the nucleotide levels, the concentrations of hypoxanthine, total and oxidized glutathione, and of conjugated dienes were measured in the intestinal tissue. The results indicate that oxygen radicals generated by xanthine oxidase are very important, but not the only significant factor in the small intestinal reperfusion damage.
D000244:Adenosine Diphosphate / Q000378:metabolism; D000249:Adenosine Monophosphate / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D002415:Cats; D005260:Female; D005978:Glutathione / Q000378:metabolism; D007022:Hypotension; D019271:Hypoxanthine; D007042:Hypoxanthines / Q000378:metabolism; D007288:Inosine / Q000494:pharmacology; D007291:Inosine Monophosphate / Q000378:metabolism; D007413:Intestinal Mucosa / Q000378:metabolism / Q000473:pathology*; D007421:Intestine, Small / Q000098:blood supply* / Q000378:metabolism; D007511:Ischemia; D008297:Male; D010084:Oxidation-Reduction / Q000187:drug effects; D013481:Superoxides / Q000378:metabolism
D007042:Hypoxanthines; D013481:Superoxides; D007291:Inosine Monophosphate; D019271:Hypoxanthine; D000249:Adenosine Monophosphate; D007288:Inosine; D000244:Adenosine Diphosphate; D000493:Allopurinol; D000255:Adenosine Triphosphate; D005978:Glutathione