丙泊酚对大鼠失血性休克复苏后复合内毒素血症致肝损伤的保护作用

The protective effect of propofol on the liver injured by hemorrhagic shock combined with endotoxin in rats

目的探讨丙泊酚对大鼠失血性休克缺血-再灌注复合内毒素血症致急性肝损伤的保护作用及其机制。方法 SD大鼠72只,随机均分为创伤组、丙泊酚组和对照组。丙泊酚组在失血性休克前30min开始以微量泵经股静脉注射1%丙泊酚10mg·kg-1·h-1,维持输注至实验结束时,创伤组和对照组以1mg·kg-1·h-1生理盐水替代。动物模型采用大鼠经股静脉放血使平均动脉压降至35～45mmHg,维持120min后回输全部失血及等量复方氯化钠进行复苏,复苏后2h再经股静脉注射内毒素5mg/kg。观察测定创伤前、失血性休克6、8h时的血浆谷丙转氨酶(ALT)活性、肝组织丙二醛(MDA)含量、肝组织超氧化物歧化酶(SOD)活性及肝组织病理学改变。结果与创伤前和对照组比较,失血后6、8h创伤组和丙泊酚组ALT活性明显升高、MAD含量明显增加(P<0.05);SOD活性明显降低(P<0.05)。与失血6h比较,失血8h创伤组ALT活性明显升高、MAD含量明显增加(P<0.05);SOD活性明显降低(P<0.05)。与创伤组比较,失血6、8h丙泊酚组ALT活性明显降低(P<0.05);MAD含量明显减少(P<0.05);SOD活性明显升高(P<0.05)。结论丙泊酚在失血性休克复苏后复合内毒素血症时能够抑制肝MDA产生和ALT活性,抑制总SOD活性的降低,减轻急性肝损伤的程度。

Objective To investigate whether or not propofol has the protective effect of on the liver injured by hemorrhagic shock combined with endotoxin and the possible mechanism of protection in rats. Methods Seventy-two healthy SD rats were randomly allocated into following groups （n=24 in each）： control group, hemorrhagic shock with endotoxin group; propofol-treatment group. The rats were loss of blood through femoral vein for 120 min until the MAP were 35-45 mm Hg, then all the blood and equal sodium were given back to recovery. 2 h later, lipopolysaccharide of 5 mg/kg were given through femoral vein. Propofol was administered intravenously in rates of propofoI-treatment groups rate of 10 mg· kg^-1 · h^-1 constantly. The levels of rnalondialdehyde and superoxide dismutase in hepatic tissue and alanine a minotrarksferase concentration in serum were measured in each rat. Results Compared with before hemorrhagic shock with endotoxin and control group, the ALT and MAD were significantly increased while SOD were obviously decreased in the hemorrhagic shock with endotoxin group and propofol treatment group after loss of blood 6 and 8 h（P〈0.05）. Compared with 6 h after loss of blood, the ALT and MAD were significantly increased while SOD were obviously decreased at 8 h after loss of blood in the hemorrhagic shock with endotoxin group （P〈 0. 05）. Compared with the hemorrhagic shock with endotoxin group, the above same thing happened to the propofol treatment group （P 〈0.05 ）. Conclusion Propofol may inhibit the production of malondialdehyde and the activity of alanine aminotransferase, suppress the decrease of superoride dismutase activity, reduce the acute liver injury after hemorrhagic shock with eudotorin through regulating the oxidant stress.