Tolerance of the cirrhotic liver to cold ischemia: ex vivo analysis in rats.

Abstract

We investigated the viability of rat cirrhotic livers preserved cold using an isolated rat liver perfusion model. Cirrhosis was induced by intravenous thioacetamide injection. Normal and cirrhotic livers were reperfused immediately or following 6 h of preservation through the portal vein with Krebs-Henseleit buffer and hyaluronic acid added. Cirrhotic livers with short cold ischemia showed higher portal venous resistance than their normal counterparts (p < 0.05), while cirrhotic livers preserved for 6 h exhibited marked elevation of the portal venous resistance as compared with their fresh counterparts or normal liver preserved cold for 6 h (p < 0.05). Similarly, the oxygen consumption of cirrhotic livers with short cold preservation was lower than that of normal livers (p < 0.05), which was further reduced by 6 h of cold preservation (p < 0.05). The bile output was not different between normal and cirrhotic livers. The sinusoidal endothelial cell function of cirrhotic livers as assessed by the clearance of hyaluronic acid was impaired even after a short period of cold ischemia. Histologically, cirrhotic livers showed severe sinusoidal endothelial cell damage, hepatocellular swelling, and marked septal edema which became more prominent by cold preservation. We conclude that the viability of the cirrhotic liver is impaired even by a short cold exposure, and that the prolongation of cold ischemia of the cirrhotic liver leads to further deterioration of the viability.