乙酮可可碱对大鼠肝脏缺血／再灌注损伤影响的实验研究

目的探讨乙酮可可碱保护大鼠肝缺血／再灌注损伤的机制。方法采取大鼠第一肝门阻断的缺血再灌注模型，将健康雄性SD大鼠64只随机分为四组：对照组及乙酮可可碱给药组，观察每组动物的病理切片，分别检测血浆谷丙转氨酶（ALT）、乳酸脱氢酶（LDH）、肿瘤坏死因子-α（TNF-α）以及肝组织匀浆中内皮素-1（ET-1）的含量，免疫组化测定P-选择素的表达。结果肝脏缺血／再灌注后，病理有明显的损伤改变。PTX保护组再灌注2、4h血清ALT、LDH、TNF-α和肝组织匀浆中ET-1含量与对照组相比显著降低（P〈0．01），PTX保护组P-选择素蛋白表达显著低于对照组（P〈0．01）。结论肝脏微循环障碍是肝脏缺血／再灌注损伤的病理基础，给予PTX预处理可降低TNF-α、ET-1产生和减少P-选择素表达，从而减轻肝脏损伤。

The Effect of Pentoxifylline on Hepatic Ischemia and Reperfusion Injury in Rats

Objective To investigate the effect of pentoxifylline（PTX） on hepatic ischemia and reperfusion injury in rats. Methods 64 healthy male SD rats were randomly divided into PTX pretreatment group and control group. Serum alanine aminotransferase（ALT）, lactate dehydrogenase（LDH）, tumor necrosis factor-a（ TNF-α and endothelin-1 of liver tissue were determined at different times. The expression of P-selectin in the liver tissue was located and analyzed by immunohistoehemical staining. Results There was histologic evidence of liver injury. At 2h, 4h of reperfusion, ALT, LDH, TNF-α and ET-1 in control group decreased compared with PTX pretreatment group（ P 〈 0.01）, Moreover, P-selectin staining was attenuated in control group compared with PTX pretreatment group（ P 〈 0.01 ）. Conclusion Activation of ET and cytokines contribute to microcirculatory disturbance, which is pathologic procedure of hepatic ischemia and reperfusion. PTX pretreatment can reduce liver injury through reducing TNF-α, ET-1 production and P-selectin expression.