卡托普利对风湿性心脏病换瓣手术病人肺缺血-再灌损伤的延迟期保护作用

Delayed protective effect of captopril on lung ischemia-reperfusion injury in valve replacement operations

目的 :研究卡托普利对风湿性心脏病换瓣手术病人肺缺血 再灌损伤的延迟期保护作用。方法 :2 0例风湿性心脏病换瓣病人被随机分为卡托普利组与对照组。卡托普利组于术前 96～ 4 8h口服 1mg·kg- 1 ·d- 1 的卡托普利片 ,对照组口服安慰剂。分别于CPB前 ,CPB后 1h ,3h ,6h ,12h测量肺血管阻力 (PVR)及肺泡—动脉血氧梯度差 (A aDO2 ) ,并于CPB前、CPB后 30min检测左、右心房血中性粒细胞 (PMN)及左房血超氧化物歧化酶 丙二醛 (SOD MDA) ,NO ,AngⅡ值。结果 :CPB后各时间点卡托普利组PVR均较对照组为低。CPB后 1h ,3h ,6h卡托普利组A aDO2 值均显著低于对照组。CPB后 30min卡托普利组右房—左房血PMN计数差值、MDA水平明显小于对照组 ,左房血SOD ,NO水平显著高于对照组。两组CPB后 30min左房血AngⅡ水平差异无显著性。结论 :风湿性心脏病换瓣病人术前 96～ 72h口服卡托普利片 (1mg·kg- 1 ·d- 1 )对病人肺组织缺血—再灌注损伤具有延迟期保护作用 。

Objective To investigate the delayed protective effect of captopril on lung ischemia reperfusion injury in patients undergoing heart valve replacement operations. Methods Twenty patients with rheumatic valve diseases were randomly divided into the captopril group and control group. The captopril group patients were pretreated with 1 mg·kg -1 ·d -1 captopril 96～48 h before the operation, whereas the control group patients were given a placebo at the same time. PVR and A aDO 2 were measured before CPB and 1 h, 3 h, 6 h, 12 h after CPB. PMN count in the left and right atrium blood and SOD/MDA, NO, AngⅡ value in the left atrium blood were also measured before and 30 min after CPB. Results PVR of the captopril group was lower than that of the control group. A aDO 2 values in the captopril group were significantly lower than those in the control group 1 h, 3 h, 6 h after CPB. The difference between the right and left atrium blood PMN was significantly lower in the captopril group than that in the control group 30 min after CPB. The left atrium blood SOD and NO value was significantly higher, whereas MDA value was significantly lower in the captopril group than that in the control group 30 min after CPB. As for AngⅡ, there was no difference between the two groups 30 min after CPB. Conclusion Captopril (1 mg·kg -1 ·d -1 ) 96～48 h before heart valve replacement operations has a delayed protective effect on lung ischemia reperfusion injury in patients with rheumatic valve diseases. The present study indicates that the protective effect may be related to the increment of endogenetic NO and the enhanced ability against lipid peroxidation.