异丙酚对体外循环肺损伤的保护作用

目的研究临床剂量异丙酚对体外循环(Extracorporeal c ircu lation,ECC)氧自由基所致的肺损伤是否有保护作用。方法选择择期30例首次心脏瓣膜置换术患者并随机分为对照组(C组)和异丙酚组(P组),每组15例。于ECC前(T1)、腔静脉开放5 m in(T2)、30 m in(T3)、60 m in(T4)时测定桡动脉血超氧化物歧化酶(SOD)、丙二醛(MDA)浓度,计算胸肺顺应性(Cs)和动态肺顺应性(Cd),呼吸指数(R I)。结果C组Cs、Cd在T2,T3,T4较T1及同时间点的P组明显下降(P<0.05),C组R I在T2,T3较T1及同时间点的P组明显升高(P<0.05),T4与T1无明显差异但仍高于P组。C组SOD T2,T3,T4显著低于P组(P<0.05),MDA显著高于P组(P<0.05)。T2,T3,T4两组MDA显著高于T1(P<0.05),但是P组升高的程度不如C组。结论临床剂量的异丙酚可能通过减少ECC氧自由基产生,增加机体清除氧自由基的能力,从而减轻ECC所致的肺脏缺血/再灌注损伤。

Protective Effect of Clinical Dose Propofol on Pulmonary Injury Induced by Extracorporeal Circulation

OBJECTIVE To study the protective effect of clinical dose propofol on pulmonary injury induced by extracorporeal circulation(ECC).METHODS Thirty patients undergoing cardiac value replacement for the first time were randomly divided into two group: control group(Group C,15 patients) and propofol group(Group P,15 patients).Pulmonary thoracic compliance(Cs),dynamic compliance(Cd) and respiratory indexes(RI) were calculated at pre-ECC(T_1),5minutes(T_2),30minutes(T_3),60minutes(T_4) after vena cava declamping.At the same time points arterial blood samples were taken for determination of SOD,MDA concentrations.RESULTS There was a significant decrease of Cs and Cd at T_2,T_3,T_4 in the group C as compared with basline values and the values of the group P respectively(P<0.05).The RI of the group C at T_2,T_3was higher than either their baseline or the values of the group P at the same measure points(P<0.05).Though there was no significant difference between at T_4 and T_1 in the group C(P<0.05),the values of the group C were higher than those of the group P at T_4(P<0.05). SOD concentration was significantly lower at T_2,T_3,T_4 in the group C than T_1 and the values of the group P respectively.There was a significant increased of MDA concentration at T_2,T_3,T_4 in the group C and the group P than T_1,but the values of group P was lower than the group C.CONCLUSION Clinical dose propofol can decrease production of oxygen free radical,and has signifucantly protective effect on the lung against pulmonary I/R injury induced by OFR during ECC.