机构地区:[1]广西医科大学第三附属医院心胸外科,南宁530031
出 处:《中国体外循环杂志》2011年第3期182-185,共4页Chinese Journal of Extracorporeal Circulation
基 金:广西科技开发项目(0015034)
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 ac id,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 canine 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 both 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.
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