Mild hypothermia during the reperfusion phase protects mitochondrial bioenergetics against ischemia-reperfusion injury in an animal model of ex-vivo liver transplantation-an experimental study

• Main Author: Martins, Rui Miguel
• Publication Date: 2019
• Other Authors: Teodoro, João S., Furtado, Emanuel, Oliveira, Rui Caetano, Tralhão, José Guilherme, Rolo, Anabela Pinto, Palmeira, Carlos Marques
• Format: Article
• Language: eng
• Source: Repositórios Científicos de Acesso Aberto de Portugal (RCAAP)
• Download full: https://hdl.handle.net/10316/107035; https://doi.org/10.7150/ijms.34617
• topic: hypothermia; mitochondria; bioenergetics; adenosine triphosphate; liver transplantation; Adenosine Triphosphate; Animals; Disease Models, Animal; Hypothermia, Induced; Liver; Liver Transplantation; Male; Membrane Potential, Mitochondrial; Mitochondria, Liver; Organ Preservation; Rats, Wistar; Reperfusion Injury; Temperature

The organ preservation paradigm has changed following the development of new ways to preserve organs. The use of machine perfusion to preserve organs appears to have several advantages compared with conventional static cold storage. For liver transplants, the temperature control provided by machine perfusion improves organ preservation. In this experimental study, we measured the effects of different temperatures on mitochondrial bioenergetics during the reperfusion phase. An experimental model of ex-vivo liver transplantation was developed in Wistar rats (Rattus norvegicus). After total hepatectomy, cold static preservation occurred at 4ºC and reperfusion was performed at 37ºC and 32ºC using a Langendorff system. We measured parameters associated with mitochondrial bioenergetics in the livers. Compared with the livers that underwent normothermic reperfusion, mild hypothermia during reperfusion caused significant increases in the mitochondrial membrane potential, the adenosine triphosphate content, and mitochondrial respiration, and a significant reduction in the lag phase (all P < 0.001). Mild hypothermia during reperfusion reduced the effect of ischemia-reperfusion injury on mitochondrial activity in liver tissue and promoted an increase in bioenergetic availability compared with normothermic reperfusion.