Background. Experimental models of warm ischemia in liver transplantation have been employed to study the mechanisms and treatment of ischemia reperfusion injury. Material. 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 postrevascularization 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). Conclusion. 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. X E PERIMENTAL MODELS of warm ischemia in liver transplantation have been employed by numerous groups to study the type and mechanisms of ischemiareperfusion injury, to assess the relation of early to eventual function of the allograft, and to test therapeutic options. 1-3 We compared two models of warm ischemia clamping the hepatic artery and portal vein for 30 minutes, and extraction of the liver 60 minutes after cardiac arrest. Both experimental models have been used by our group in previous studies. [4][5][6] The comparisons included a group control in which the graft liver experienced no ischemia.

COMPLEMENT is gradually being considered in ischemia-reperfusion, especially in xenotransplantation. [1][2][3][4][5] Reperfusion injury is characterized by deposition of C3 and C5b-9. 1 Complement inhibitors are used in amelioration of warm ischemia 1,2 and rejection episodes. 3 Tranexamic acid (Amca), a synthetic antifibrinolytic agent, has proven to be effective in acquired angioedema (a deficiency of the C1 inhibitor [Ci-inh]). 6 Because of the increased risk of severe fibrinolysis, Amca is often used during orthotopic liver transplantation (OLT). 7 Although no report of the use of Amca was found in the treatment of ischemia-reperfusion injury, the anticomplement effect of Amca has been demonstrated. 8 Our aim was to study the complement activation and the effect of Amca on complement and ischemia-reperfusion injury in a liver allograft with donor warm ischemia. MATERIALS AND METHODSTwenty-one liver transplants were performed on Large White pigs. In all donors, the hepatic blood supply was occluded for 30 minutes before the extraction. The animals were divided into two groups, according to the treatment received by the recipients: the control group (n = 11) did not receive Amca and the Amca group (n = 10) received a single intravenous (IV) dose of 500 mg of Amca at the beginning of the OLT. Total complement activity (CH100) and C1-inh were measured at the beginning of OLT, in the preanhepatic phase, 1 minute prerevascularization, and 5, 15, and 30 minutes postrevascularization. Blood samples were extracted from the jugular vein during the OLT and the following 3 days and also from the portal vein (only for CH100) during the OLT. Blood was extracted for liver function tests (alanine transaminase [ALT], aspartate transaminase [AST], total bilirubin, lactate dehydrogenase [LDH], alkaline phosphatase) and coagulation studies (prothrombin time, partial thromboplastin time, thrombin time, and fibrinogen) at the beginning of OLT, at the end, at 6 hours post-OLT, at 24 hours, and thereafter daily. We determined malondialdehyde (MDA) concentrations in the hepatic tissue at the beginning in the donor (initial), at the end of OLT (postreperfusion), and on the third day. Statistical analysis was performed with SPSS statistical software

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