山莨菪碱对兔急性心肌梗死再灌注后梗死面积的影响

Effects of Anisodamine on the Area of Myocardial Infarction in Reperfusion Injured Rabbits After Acute Myocardial Infarction

目的:探讨山莨菪碱预处理对急性心肌梗死后再灌注损伤的保护作用及其机制。方法:采用结扎冠状动脉左前降支3 h后再开放60 min的方法建立兔急性心肌梗死再灌注模型。20只兔随机分为4组,A组:急性心肌梗死再灌注组;B组:山莨菪碱(5 mg/kg)+急性心肌梗死再灌注组;C组:格列本脲(5 mg/kg)+急性心肌梗死再灌注组;D组:格列本脲+山莨菪碱+急性心肌梗死再灌注组。再灌注结束后测定各组血清肌酸激酶同工酶(CK-MB)活性,应用20%伊文思蓝及1%氯化三苯四唑啉染色后计算心肌梗死面积。结果:B组血清CK-MB活性较A组显著降低(P<0.01),C组与A组比较差异无统计学意义(P>0.05),D组血清CK-MB活性较A组显著降低(P<0.05),但仍高于B组(P<0.05)。B组心肌梗死范围较A组和C组显著减少(P<0.01),C组与A组相似(P>0.05),D组较A组显著减少(P<0.05),但仍明显高于B组(P<0.05)。结论:山莨菪碱可明显降低血清CK-MB活性、减小心肌梗死面积,对急性心肌梗死再灌注损伤具有保护作用,机制可能与山莨菪碱激活ATP敏感性钾通道有关。

Objective ：To investigate the effects and mechanism of the pretreatment with anisodamine on the area of myocardial infarction in reperfusion injured rabbits after acute myocardial infarction （AMI）. Methods：Twenty New Zealand white rabbits were randomly divided into four groups：group A, AMI/reperfusion; group B, treated with anisodamine （5 mg/kg）before AMI; group C, treated with glibenclamide （5 mg/kg）before AMl;group D, treated with glibenclamide and anisodamine before AMI. Models of AMI/reperfusion were established by 180- minute of coronary occlusion and 60- minute of reperfnsion. Ischemic myocardium at risk was assessed with Azovan Blue dye and infarct size with TTC（ 1% ）staining and creatine kinase-MB（CK-MB）. Results ：The serum content of CK-MB and the infarct size were significantly lower in group B than those in group A （ P 〈 0.01 ） ; there was no difference of statistical significance between group C and A （ P 〉 0.05 ）, however,activation of CK-MB were markedly lower in group D than that of group A （ P 〈 0.05 ） , and significantly higher than that of group B （ P 〈 0. 05）. The infarct size of group B were significantly reduced when compared with that of group A and C （P 〈 0. 01 ） ;there were similar between group A and C （ P 〉 0.05 ） ; they were obviously lower in group D than that of group A （ P 〈 0. 05 ）, but higher than that of group B （ P 〈 0.05 ）. Conclusion：Anisodamine can significantly reduce myocardial infarction size during AMI and reperfusion in rabbits,and the activation of ATP-sensitive K channels might be involved in this orotective mechanism.