脂微球前列腺素E1对体外循环心脏瓣膜置换术患者肺保护的初步探讨

Protective effect of lipo-prostaglandin E1 against lung injury in patients of cardiac vale replacement during cardiopulmonary bypass

目的探讨静脉应用脂微球前列腺素E1(Lipo-PGE1)在心脏瓣膜置换术患者体外循环(CPB)术中的肺保护作用及可能的机制。方法42例首次心脏瓣膜置换术患者,随机分为Lipo-PGE1组(P组,n=21),CPB开始即从中心静脉持续泵入和预充液中加入Lipo-PGE110ng/mL;对照组(C组,n=21),CPB中给予等量生理盐水。分别于CPB前、腔静脉开放后10min、停机和术毕4个时点,采集桡动脉血行血气分析,监测吸入氧浓度、气道峰压、潮气量并计算氧合指数(OI),呼吸指数(RI),肺动态顺应性(Cd);测定左右心房血中性粒细胞数量,计算肺内中性粒细胞滞留数(PMNn);同期测定桡动脉血中白细胞介素(IL)-8浓度的变化。结果C组OI和肺Cd在体外循环停机后至术毕较CPB前均明显降低(P<0.05),而P组OI和肺Cd水平明显优于C组(P<0.05);C组在腔静脉开放后RI明显升高(P<0.05),而P组病人RI在腔静脉开放后至术毕较C组显著降低(P<0.05)。两组病人腔静脉开放后,左右心房血PMN计数均较CPB前明显增加(P<0.05);C组病人肺内PMNn在腔静脉开放后10min至术毕均显著增加,而P组病人增加不明显,两组比较差异有统计学意义(P<0.05);C组病人各时点IL-8浓度明显增加,而P组增加不明显,与C组比较差异有统计学意义(P均<0.05)。结论CPB中使用Lipo-PGE1能抑制PMN激活,减少PMN肺内滞留及IL-8的释放,发挥明显的肺保护作用。

[Objective ] To study the protective effect of Liposoma-prostaglandin E1 （Lipo-PGE1） against lung injury during eardiopulmonary bypass （CPB） and as well as the possible mechanism. [Methods] Patients scheduled for cardiac value replacement for the first time were randomized into two groups： control group （C group） and Lipo- PGEl-treated group （P group）. In P group Lipo-PGE1 10 ng/kg/min was given at the beginning of CPB and 10 ng/ mL was added in primiing fluid; while in control group normal saline was given instead of Lipo-PGE1. Pulmonary dynamic compliance （Cd） were measured at pre-CPB, 10 minutes after declamping of vena cava, at termination of CPB and at the end of operation. At the same time points arterial and mixed venous blood samples were taken for determination of polymorphonuclear leukocyte （PMNa, PMNv） count, intrapulmonaryn PMN trapping, blood gas analysis, calculation of oxygenation index （OI） and respiratory indexes （RJ）. Meanwhile, the level of arterial interleukin-8 were measured. [ Results ] Compared with the baseline valves, OI and Cd in control group were significantly deteriorating after vena cava declamping （P 〈0.05）, while in P group no significant changes were seen. In C group, RI was significantly increased during and post-CPB and markedly lower in P group （P 〈0.05）. In both groups PMN count in arterial and mixed venous blood were significantly increased after vena cava declamping. In C group the intrapulmonary PMN trapping was increased at 10rain after vena cava declamping as compared with the baseline （P 〈0.05）. While in P group no significant changes were seen and the intrapulmonary PMN trapping was significantly lower in P group than in C group （P 〈0.05）. The plasma level of IL-8 in C group was increased significantly during and post- CPB （P〈0.05）; whereas, in P group the level of IL-8 was markedly lower than that in C group （P 〈0.05）. [ Conclusion] Lipo-prostaglandin E1 can obviously reduce lung injury during CPB by inhibiting activation of PMN, decreasing PMN trapping and IL-8 releasing.