论文部分内容阅读
目的探讨异丙酚对肝缺血再灌注损伤犬肝细胞线粒体的作用及其机制。方法20只杂种犬随机分为4组(n=5):假手术组(S组)、缺血再灌注组(I／R组)、小剂量异丙酚组(P1组)及大剂量异丙酚组(P2组)。以10ml／min速率静脉输注6％羟乙基淀粉150～200ml,同时从股动脉缓慢放血100～150 ml,使平均动脉压(MAP)不低于85 mm Hg。S、I／R组静脉注射3％戊巴比妥钠30 mg／kg、维库溴铵0．3mg／kg麻醉诱导,P1、P2组依次静脉注射异丙酚6mg／kg、维库溴铵0．3mg／kg麻醉诱导,气管插管后控制呼吸。S、I／R组间断静脉注射戊巴比妥钠维持麻醉,P1、P2组以血浆靶浓度6、12μg／ml靶控输注异丙酚维持麻醉30 min后麻醉维持同S组。缺血期间回输自体血,维持MAP不低于80 mm Hg。I／R、P1组、P2组气管插管后30 min制备肝缺血(缺血30 min)再灌注模型。分别于缺血前即刻、缺血30 min、再灌注60 min抽取静脉血,测定血浆谷丙转氨酶(ALT)、谷草转氨酶(AST)及肝细胞线粒体Na+-K+-ATP酶活性,并在透射电镜下观察肝细胞线粒体的超微结构。结果肝缺血再灌注可导致血浆ALT、AST活性升高,肝细胞线粒体Na+-K+-ATP酶活性降低,肝线粒体损伤,异丙酚可减弱肝缺血再灌注导致的上述改变,以大剂量效果较好。结论异丙酚可减轻肝缺血再灌注损伤犬肝细胞线粒体损伤,呈剂量依赖性。
Objective To investigate the effect and mechanism of propofol on mitochondria of hepatic cells in liver ischemia-reperfusion injury in dogs. Methods 20 mongrel dogs were randomly divided into 4 groups (n = 5): sham operation group (S group), ischemia reperfusion group (I / R group), low dose propofol group (P1 group) Propofol group (P2 group). Infusions of 150-200 ml of 6% hydroxyethyl starch at a rate of 10 ml / min and 100-150 ml of blood from the femoral artery were slowly bled to a mean arterial pressure (MAP) of not less than 85 mm Hg. S and I / R groups were injected intravenously with 3% sodium pentobarbital 30 mg / kg and vecuronium 0.3 mg / kg, respectively. Groups P1 and P2 received intravenous propofol 6 mg / kg and vecuronium Anesthesia was induced at 0.3 mg / kg and respiration was controlled after tracheal intubation. S, I / R group intermittent intravenous injection of sodium pentobarbital to maintain anesthesia, P1, P2 group to plasma target concentration of 6,12μg / ml target-controlled infusion of propofol to maintain anesthesia for 30 min after anesthesia with the S group. Autologous blood was transfused during ischemia, maintaining a MAP of at least 80 mm Hg. I / R, P1 group, P2 group were prepared 30 min after tracheal intubation of hepatic ischemia (ischemia 30 min) reperfusion model. Venous blood was collected immediately before ischemia, 30 min after ischemia, and 60 min after reperfusion. The activities of alanine aminotransferase (ALT), aspartate aminotransferase (AST) and mitochondrial Na + -K + -ATPase in liver cells were measured. Observe the ultrastructure of hepatocyte mitochondria. Results Hepatic ischemia-reperfusion could lead to the increase of plasma ALT and AST activity, decrease of mitochondrial Na + -K + -ATPase activity and hepatic mitochondrial damage in liver cells. Propofol attenuated the above changes induced by hepatic ischemia-reperfusion, The effect is better. Conclusion Propofol can reduce the damage of hepatocyte mitochondria in liver ischemia-reperfusion injury in a dose-dependent manner.