Brain death does not affect hepatic allograft function and survival after orthotopic transplantation in a canine model

• Published in: Transplantation Vol. 73; no. 8; p. 1218
• Main Authors: Compagnon, Philippe, Wang, Hongbing, Lindell, Susanne L, Ametani, Mary S, Mangino, Martin J, D'Alessandro, Anthony M, Southard, James H
• Format: Journal Article
• Language: English
• Published: United States 27.04.2002
• Subjects: Adenosine; Allopurinol; Animals; Aspartate Aminotransferases - metabolism; Blood Pressure; Brain Death - physiopathology; Dogs; Electroencephalography; Female; Glutathione; Graft Survival - physiology; Heart Rate; Hemodynamics - physiology; Insulin; L-Lactate Dehydrogenase - metabolism; Liver; Liver Function Tests; Liver Transplantation - physiology; Models, Animal; Organ Preservation - methods; Organ Preservation Solutions; Raffinose; Reference Values; Transplantation, Homologous
• ISSN: 0041-1337
• DOI: 10.1097/00007890-200204270-00006

Brain death has been shown to decrease graft function and survival in rodent models. The aim of this study was to evaluate how brain death affects graft viability in the donor and liver tolerance to cold preservation as assessed by survival in a canine transplant model. Beagle dogs were used for the study. Non-brain dead (BD) donors served as controls. Brain death was induced by sudden inflation of a subdural balloon catheter with continuous monitoring of arterial blood pressure and electroencephalographic activity. Sixteen hours after confirmation of brain death, liver grafts were retrieved. All livers were flushed in situ and preserved for 24 hr in cold University of Wisconsin solution before transplantation. Recipient survival rates, serum hepatic enzyme levels, coagulation, and metabolic parameters of the recipients were analyzed. No significant changes were observed in serum aminotransferases (alanine and aspartate transaminases) and lactate dehydrogenase levels in the BD donor. After preservation, control (n=6) and BD livers (n=5) showed full functional recovery after transplant with 100% survival in both groups at day 7. There was no significant difference in peak serum alanine, aspartate transaminases, and lactate dehydrogenase after transplantation in recipients who received a liver from BD donor compared to control group. BD livers were functionally as capable as control livers in correcting metabolic acidosis during the first 24 hr posttransplantation. Coagulation profiles (index normalized ratio, activated partial thromboplastin time) after reperfusion were similar between groups. In contrast to previous reports in rodent models, our study shows that brain death does not cause significant liver dysfunction in the donor before organ removal. Donor brain death and prolonged liver graft preservation do not interact significantly to impair liver function and survival after transplantation.