[Experimental study of injury on the small intestine in acute portal vein occlusion and the following restoration of portal vein flow in rats--hemodynamics and lipid peroxidation].
This study was performed to clarify the relationship between hemodynamics, congestive damage, lipid peroxidation and intraluminal hemorrhage of the small intestine. Using 51Cr-red blood cells, with a temporary occlusion of the portal vein for 30 min. in rats, the hemodynamic, biochemical and histological changes were investigated. By occluding the portal vein, its pressure increased to a level eight times higher than normal, and destruction of the intestinal mucosa and an increase of TBA reactants were observed. The intraluminal hemorrhage of the intestine increased to a quantity 7.5 times higher than usual during portal vein occlusion, and it decreased gradually after reperfusion. At 120 min. after reperfusion, this amount remained high, but the administration of Allopurinol diminished its level. A technique of temporary simultaneous occlusion of the superior mesenteric artery or the bypass between the portal and jugular veins was effective in reducing the congestive damage on the intestine. During the occlusion of the portal vein, sudden and high pressure of the portal vein primarily causes congestive damage, and superoxide generated by a xanthine oxidase system during reperfusion may cause lipid peroxidation which induces reperfusion injury. Thus, the lipid peroxidation may accelerate the injury on the small intestine.
Ueda
S
S
Second Department of Surgery, Ehime University School of Medicine, Japan.
D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D006471:Gastrointestinal Hemorrhage / Q000209:etiology*; D006439:Hemodynamics; D007421:Intestine, Small / Q000378:metabolism / Q000473:pathology*; D015227:Lipid Peroxidation; D008297:Male; D011169:Portal Vein / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D015427:Reperfusion Injury / Q000209:etiology*
D000493:Allopurinol