Pathophysiological changes caused by occlusion of blood flow into the liver during hepatectomy in dogs with obstructive jaundice: effects of intestinal congestion.

Obstructive jaundice was produced in adult mongrel dogs by cholecystectomy and ligation of the common bile duct. Two weeks later 40% hepatectomy was performed during 10 min occlusion of hepatic inflow (group I). Liver tissue lipid peroxide levels increased significantly and superoxide dismutase activity decreased. The portal endotoxin (Et) concentration increased markedly after reperfusion and peripheral blood Et and serum beta-N-acetyl hexosaminidase levels increased markedly, beginning 3 h after reperfusion. The phagocytic index increased transiently after reperfusion, but decreased markedly thereafter. Hepatocyte degeneration and necrosis became severe, intestinal villi were damaged and the 1 week survival rate was 23.1%; deaths were due to liver failure. These changes were prevented by construction of a portosystemic bypass and a 1 week survival rate of 70% (group II) was achieved. When the ischaemic time was prolonged to 20 min with the portosystemic bypass (group III), the pathological changes resembled those seen in group I, although no changes were observed in portal or peripheral blood Et levels. These findings suggest that major hepatectomy in the presence of severe jaundice should be carefully performed so that the ischaemic time is minimized during portosystemic bypass in an attempt not only to prevent production of Et in portal venous blood due to intestinal congestion, but also to reduce ischaemia-reperfusion injury.