乌司他丁对体外循环下犬心肌保护作用的实验研究

摘要

目的 研究乌司他丁(UTI)应用于体外循环(CPB)中对犬心肌组织中细胞间黏附分子-1(ICAM-1)表达的影响及其对心肌的保护作用.方法 试验用杂种犬20只,随机平均分为乌司他丁实验组(U组)和对照组(C组),每组各10只.U组在CPB预充液中加1万U/kg UTI,并于CPB转机开始前即经静脉再给1万U/kg UTI持续滴注.C组常规建立CPB并转机.分别于CPB转机前10 min(A时点)和转机后60 min(B时点)两个时点,切取犬心肌右心耳组织,检测心肌组织ICAM-1表达量及心肌组织中超氧化物歧化酶(SOD)、丙二醛(MDA)、乳酸(Lactic acid,LA)、三磷酸腺苷酶(ATPase)的水平.并记录CPB建立时间、主动脉阻断时间、主动脉灌注时间、CPB转机时间、心脏复跳情况.结果 两组实验犬心肌组织中,ICAM-1的表达量在B时点较A时点均明显增高,但在B时点 U组ICAM-1表达量低于C组(P<0.05); LA 和MDA 的含量在B时点均明显高于A时点,但在B时点U组LA和MDA的含量均低于C组(P<0.05);SOD和ATPase的活力在B时点均低于A时点,但在B时点U组SOD和ATPase的活力高于C组(P<0.05).结论 CPB时,心肌组织的缺血-再灌注损伤可引起心肌组织ICAM-1 表达上调,心肌组织中 LA和MDA含量增高,SOD和ATPase活力降低.应用乌司他丁可抑制心肌组织中ICAM-1的表达,减少心肌组织中LA和MDA 的产生,降低SOD和ATPase的消耗,从而减轻心肌的炎症反应,进而保护心肌组织.%OBJECTIVE To investigate the expression of intercellular adhesion molecule - 1( ICAM - 1 ) in canine myocardium during the cardiopulmanory bypass ( CPB ) , evaluate whether ulinastatin could influence its expression and the protective effect on myocardium. METHODS Twenty dogs were randomly and divided into two groups: ulinastatin group ( UG ) and control group ( CG ). In ulinastatin group ( U n = 10 ) dogs received ulinastatin 20000 unit/kg, half dose was added into the CPB priming fluid, and another half dose was given by intravenous injection before CPB running. In control group ( C n = 10 ) dogs received CPB conventionally, the same volume of saline instead of ulinastatin. Right atrial appendage of the dog was obtained by the time of 10 minitures before CPB running ( point A ) and 60 minitures after CPB running ( point B ). The expression of ICAM - 1 in cardiac myocytes and the levels of SOD, MDA, LA, ATPase in camne myocardium were detected. And meantime the establishment and running time of CPB, aortic cross clamp time, heart re - beat were recorded. RESULTS The expression of ICAM - 1 in myocardial tissue after CPB in both groups increased and it was higher in control group than that in ulinastatin group ( P ＜0. 05 ). The levels of LA and MDA in myocardial tissue after PCPS in both groups increased and they were higher in control group than that in ulinastatin group ( P ＜ 0. 05 ). The levels of SOD and ATPase in myocardial tissue after CPB in hoth groups decreased and higher in ulinastatin group than that in control group ( P ＜0.05 ). CONCLUSION Myocardial ischemic reperfusion injury can cause the expression of ICAM - 1 in myocardium highly up - regulating, the levels of LA and MDA in myocardial tissue increasing, SOD and ATPase decreasing. Ulinastatin can restrain the expression of the ICAM - 1 . reduced the productions of LA and MDA, and decrease the consumption of SOD and ATPase in myocardial tissue during the CPB , thus protecting the myocardial tissue by inhibiting the myocardial inflammation.