目的 观察肝脏缺血再灌注后急性肾损伤的发病机制及丙泊酚的保护作用.方法 成年封闭群SD雄性大鼠40只,随机分为:假手术(Sham)组;缺血再灌注2 h(IR2)组;缺血再灌注6 h(IR6)组; 丙泊酚2 h(P2)组;丙泊酚6 h(P6)组.P组自缺血前30 min静脉输注丙泊酚1 mg/(kg·min),Sham组及IR组按0.1 ml/(kg·min)速率输注乳酸钠林格氏液,时间30 min.在相应的时间点处死动物,测定尿素氮(BUN)、肌酐(Cr)、肿瘤坏死因子-α(TNF-α)、超氧化物岐化酶(SOD)、丙二醛(MDA)的含量以及Na+-K+ -ATP 酶、Ca2+-ATP 酶活性.结果 IR组及P组大鼠缺血再灌注后BUN、Cr、TNF-α的水平较sham组明显升高,但P组再灌注2 h、6 h时均明显低于IR组.Sham组SOD水平与P组相比无明显差异.IR各组SOD值均显著降低,P组SOD值与IR组相比明显升高.在大鼠肝脏缺血/再灌注后,IR组MDA值较P组及Sham组均显著升高,P组MDA轻度升高,与Sham组相比无明显差异.IR组大鼠的Na+-K+ -ATP 酶、Ca2+-ATP 酶活性明显低于Sham组及P组.结论 丙泊酚通过抑制炎症因子的分泌,减轻氧化应激损伤等机制,对肝脏缺血再灌注损伤后肾脏的继发性损伤有明显的保护作用.%Objective To study the mechanism of acute renal impairment occurred after hepatic ischemia / reperfusion and the protective effect of propofol. Methods Forty male SD rats were randomly divided into sham group; IR2 group ( ischemia with reperfusion for2 hr ), IR6 group ( ischemia with reperfusion for 6 hr ); P2 group ( propofol for 2h ) and P6 group ( propofol for 6 hr ) ; and 1 mg/( kg · min )propofol was infused within 30 min before ischemia in P groups, and same volume of sodium lactate Ringer's solution was infused in Sham and IR groups. Blood concentrations of BUN, Cr,TNF - α, SOD, MDA and activities of Na + - K + - ATPase and Ca2 + - ATPase were examined at points of 2 and 6 hours after reperfusion. Results Blood concentrations of BUN, Cr, TNF - α and MDA were significantly elevated after reperfusion in IR and P groups. But these figures in P groups were lowered than those of IR groups; levels of SOD and activities of Na + -K + -ATPase and Ca2 + -AT-Pase in P groups were higher than those of IR groups. Conclusion Acute renal impairment followed hepatic ischemia / reperfusion is mainly induced by oxidant stress and neutrophil infiltration in renal tissue. Propofol may have the effect of antioxidation and decreasing infiltration of neutrophils, hence it can attenuate the renal impairment induced by hepatic ischemia / reperfusion.
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