肝脏缺血再灌注损伤与肝微循环变化

肝脏缺血再灌注见于许多临床疾病和手术过程中。肝缺血再灌注时，肝脏组织细胞发生一系列代谢、结构和功能的损伤，甚至导致肝功能衰竭，是影响疾病预后、手术成败和病人存活的主要因素之一。因此研究肝缺血再灌注损伤和防治具有重要的临床意义。目前有关常温肝缺血再灌注损伤与肝微循环变化的关系有待研究，本实验对此进行初步观察，为防治肝缺血再灌注损伤提供理论依据。１　材料与方法１．１　动物模型与分组健康Ｗｉｓｔａｒ大鼠，雌雄兼用，体重２００～２５０ｇ。禁食１２ｈ后，腹腔注射３％戊巴比妥钠３００ｍｇ／ｋｇ（体重）施行麻…

Liver Ischemia Reperfusion Injury and Changes of Liver Microcirculation

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.