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Abstract

Experimental models of warm ischemia in liver transplantation have been employed to study the mechanisms and treatment of ischemia reperfusion injury. METHODS: We compared a control group without (group A, n = 10) versus two models of warm ischemia of liver transplants in pigs: namely, occlusion of the hepatic artery and portal vein for 30 minutes (group B, n = 23) and extraction of the liver 60 minutes after cardiac arrest (group C, n = 5). Liver function tests, coagulation studies, and liver biopsies were performed during the first 24 hours post-liver transplant. RESULTS: Clamping of the hepatic vasculature in group B produced a significant liver injury compared with the control group: elevation of the ALT and an abnormal 1-hour post-revascularization biopsy similar to that observed in the cardiac arrest group C. The transaminase levels were lower among group A animals (P <.05). But the hepatic synthetic functions as reflected in the protrombin time (PT) were not affected in group B versus group A. The alteration in PT with respect to the initial value was similar among group A and group B animals, which were significantly less than that in group C (P <.05). CONCLUSIONS: Occlusion of the hepatic artery and portal vein, a simple surgical maneuver, causes moderate damage to a liver graft but less alteration of hepatic synthetic function. Clamping of the hepatic vasculture obtains more long-term survivors after OLT than cardiac arrest.

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