Objective: To assess the relationship between liver ischemia reperfusion injury and the changes of liver microcirculation. Methods: A model of normothermic hepatic blood flow clamping and declamping in rat was adopted. The animals survived, alamine aminotransferase serum(SALT) level, extent of hepatic necrosis, liver volume of blood flow and ultrastructure of liver sinusoids during various periods of ischemia and reperfusion were observed comparatively. Results: The mortality in group of false operation, ischemia for 20, 40, 60 and 90 minutes was 0%, 5%, 10%, 85% and 95% respectively; and animals died with a high SALT level. After 20, 40, 60 or 90 minutes ischemia and 120 minutes reperfusion, the ratio of necrotic to no necrotic liver were 3.9% , 13.5% , 66.4% or 82.7% , of those the percentage necrosis during reperfusion 120 minutes was 7.7% , 11.1% , 68.1% or 67.2% respectively; The liver volume of blood flow decreased to 94.7% , 85.3% , 55.9% or 43.5% of normal values in end of ischemia; Liver sinusoidal obstruction by blebs originating from the hepatocytes, fragments of sinusoidal endothelial cell damage and aggregation of blood cells was observed in group of 60, 90 minutes ischemia. Conclusions: Liver ischemia can result in cellular injury from ischemia itself, but an addition component of injury results from events occurring during reperfusion after lengthening of the ischemia, and show that reperfusion injury was attributed to the microcirculatory disturbance, decreasing liver blood flow, increasing rapidly the degree of irreversible damage and mortality.
