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机构地区:[1]华中科技大学同济医学院附属协和医院心脏外科,武汉430022
出 处:《中华实验外科杂志》2006年第12期1476-1477,I0021,共3页Chinese Journal of Experimental Surgery
摘 要:目的探讨特异性Na+/H+交换抑制剂卡立泊来德(Cariporide)加入停搏液中对缺血再灌注心肌的保护作用。方法20只SD雄性大鼠随机分成2组(每组10只),即对照组(停搏液为改良St.ThomasⅡ停搏液)和实验组(停搏液为加入Cariporide的改良St.ThomasⅡ停搏液)。离体鼠心在改良Langendorff灌注模型上30 min预灌注,60 min停搏,30 min再灌注,监测心脏缺血前及复灌后血流动力学变化,心肌酶CK-MB、LDH变化,电镜观察心肌超微结构改变,评价心肌保护效果。结果再灌注后,实验组心功能、心肌超微结构的改善明显优于对照组;心肌酶CK-MB、LDH的漏出明显低于对照组(P<0.05)。结论特异性Na+/H+交换抑制剂Cariporide作为停搏液的辅剂可显著减轻心肌缺血再灌注损伤,改善低温缺血心肌的功能恢复。Objective To assess the cardioprotective efficacy of Cariporide as an adjunct to cardioplegia on myocardial ischemia-reperfusion injury in rats. Method Twenty male Sprague-Dawley rat hearts were randomly divided into 2 groups (n = 10): a control group and a treatment group with Carlporide as an adjunct to cardioplegia. After control perfusion in Langendorff mode with Krebs-Henseleit bi- carbonate buffer (KHB) for 30 minutes,the isolated rat hearts were infused with cardioplegia (without or with Cariporide) for 2 minutes to produce cardiac arrest and subjected to 60 minutes of 17℃ arrest. Sixty minutes after the ischemic arrest, then the hearts were reperfused with KHB for 30 minutes. The hemodynamic parameters and the level of creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH) of coronary venous sinus solution were measured before ischemia and during reperfusion. Myocardial and mitochondrial ultrastruetures were observed under electronmicroscope. Results Application of Cariporide as an adjunct to cardioplegia improved significantly recovery of cardiac function and decreased the level of CK-MB, LDH of coronary venous sinus solution (P 〈 0.05 ),the myocardial tissues had more normal ultrastructures. Conclusions Our results suggest that Cariporide supplement in cardioplegia alleviate the reperfusion mediated myocardial injury.
关 键 词:CARIPORIDE 再灌注损伤 心肌保护
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