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目的探讨依托咪酯(etomidate)预处理对肝脏缺血再灌注损伤细胞凋亡的影响。方法 20只杂种犬随机分组(n=4):假手术组、缺血再灌注组、小剂量依托咪酯预处理组、大剂量依托咪酯预处理组,开放液路,监测平均动脉压(MAP),用3%戊巴比妥钠30mg/kg静注间断给药维持麻醉,静注维库溴铵0.3mg/kg,气管插管后控制呼吸。缺血再灌注组、小剂量依托咪酯预处理组、大剂量依托咪酯预处理组分别于肝缺血前30min静注生理盐水,依托咪酯0.6mg/kg(低浓度),依托咪酯1.5mg/kg(高浓度),阻断肝第一、第二肝门建立肝缺血再灌注模型。除Sham组外,所有犬肝脏都经历30min缺血和120min再灌注。再灌注120min时,取各组缺血区肝脏组织,TUNEL法测定肝脏细胞的凋亡情况,免疫组化法测定各组Bcl-2和Bax的表达。结果TUNEL肝细胞凋亡:高浓度治疗组明显低于缺血组和低浓度治疗组(P<0.05);BCL-2蛋白表达:高浓度治疗组明显高于缺血组和低浓度治疗组(P<0.05);BAX蛋白表达:高浓度治疗组与低浓度治疗组明显低于缺血组和假手术组(P<0.05)。结论依托咪酯预处理可上调Bcl-2蛋白表达,下调Bax蛋白的表达,抑制肝细胞凋亡,减轻缺血再灌注损伤。
Objective To investigate the effect of etomidate on the apoptosis of liver cells during ischemia-reperfusion injury. Methods 20 mongrel dogs were randomly divided into four groups: sham operation group, ischemia reperfusion group, low dose etomidate preconditioning group, high dose etomidate preconditioning group, open fluid passage, mean arterial pressure monitoring (n = MAP) with intermittent administration of 3% sodium pentobarbital 30mg / kg intravenously to maintain anesthesia, intravenous vecuronium 0.3mg / kg, after intubation to control breathing. Ischemia reperfusion group, low dose etomidate preconditioning group and high dose etomidate preconditioning group were injected with normal saline, etomidate 0.6mg / kg (low concentration), etomidate 1.5mg / kg (high concentration), blocking the liver first and second liver to establish a model of liver ischemia-reperfusion. Except for the Sham group, all canine livers experienced 30 min ischemia and 120 min reperfusion. At 120 min after reperfusion, the liver tissue of ischemic zone of each group was taken out. The apoptosis of liver cells was measured by TUNEL method. The expressions of Bcl-2 and Bax in each group were determined by immunohistochemistry. Results The apoptosis of TUNEL hepatocytes was significantly lower in the high concentration group than in the ischemic group and the low concentration group (P <0.05). The expression of BCL-2 protein in the high concentration group was significantly higher than that in the ischemic group and the low concentration group P <0.05). The expression of BAX protein in high concentration group and low concentration group were significantly lower than those in ischemia group and sham operation group (P <0.05). Conclusion Etomidone can up-regulate Bcl-2 protein expression, down-regulate the expression of Bax protein, inhibit hepatocyte apoptosis and reduce ischemia-reperfusion injury.