weaned from cardiopulmonary bypass support. In both cases, the grafts rejected within minutes. There have been numerous attempts to support patients with fulminant hepatic failure using ex vivo perfusion of liver xenografts. In most of these cases, pig livers were used. Routinely, antibodies to pig serum proteins developed and titres of antipig antibodies increased. These livers were functional, and demonstrated the ability to clear lactate and ammonia and to synthesize donor proteins for many hours. Porcine livers appear to be less susceptible to antibody-mediated graft damage than other porcine organs perfused by human blood, suggesting and inherent resistance to antibody-mediated graft damage. This is similar to observations made in clinical ABO-incompatible liver transplants.

Makowka et al transplanted a pig liver into a young woman with fulminant hepatic failure, with the intent of using it as a 'bridge' until a human liver became available. Pretransplant, the recipient's blood was perfused ex vivo through the pig's kidneys to absorb antipig antibodies. Posttransplant, antipig antibodies rapidly rebounded, perhaps induced by the administration of unabsorbed blood products to the patient. Immunopathological evidence of graft rejection occurred in about three hours, and the patient died before successful bridging to an allograft could be achieved. Pathological analysis of the xenograft revealed diffuse vascular thrombosis, haemorrhagic necrosis, and extensive infiltration by neutro-phils. Vascular deposits of IgG, IgM, and complement components were found. These results corroborate laboratory studies demonstrating the importance of antibody, complement, and elements of acute inflammatory reaction during HAR.

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