【摘要】 目的:评价急性心肌梗死(AMI)再灌注后血管性假血友病因子(vWF)的变化及腺苷对vWF的影响,探讨无再流的可能机制。方法:中华小型猪24只,随机分成对照组、腺苷治疗组和假手术组,每组8只。冠状动脉结扎3h,松解1h制备AMI再灌注模型。酶联免疫吸附双抗体夹心法(ELISA)测定AMI前、后和再灌注后血浆vWF的含量;采用免疫印迹、免疫组化和RT-PCR的方法观察正常、缺血和无再流区心肌组织内vWF及其mRNA的表达。结果:(1)对照组AMI后3h、再灌注后5min和1h的血浆vWF水平均显著高于AMI前(均P<0.01),且升高幅度均相当(均P>0.05)。而腺苷组3个时点的vWF升高幅度均显著低于对照组(均P<0.05)。(2)对照组和腺苷组一样,缺血区和无再流区心肌组织中vWF表达均显著高于正常区心肌组织(均P<0.01),且无再流区vWF表达升高比缺血区均更显著(均P<0.01)。两组间对比,腺苷组仅缺血区心肌组织中vWF表达显著低于对照组(P<0.01)。(3)对照和腺苷两组缺血区心肌组织中vWF的mRNA表达均显著高于正常区心肌组织(均P<0.01),而无再流区心肌组织中vWF的mRNA表达均显著低于正常区心肌组织(均P<0.01)。两组间对比,腺苷组仅在缺血区上调幅度显著低于对照组(P<0.01)。结论:心肌微血管内皮细胞受损可能是AMI再灌注后无再流发生的重要机制之一,腺苷可能也通过保护内皮细胞起到了减少无再流的作用。更多还原

【Abstract】 AIM:Adenosine is experimentally and clinically effective in preventing even reversing myocardial infarction no-reflow,though the mechanisms are still not to be verified.This study was sought to evaluate the effect of adenosine on von willbrand factor(vWF)in the infarcted reflow and no-reflow myocardium of mini-swines.METHODS:Twenty-four animals were randomized into 3 study groups:8 in controls,8 in adenosine-treated and 8 in sham-operated.The mini-swines were subjected to 3 hours of coronary occlusion followed by 60 minutes of reperfusion except those in the sham-operated group.The normal,infracted reflow and no-reflow myocardium was divided after experiment.vWF in both blood sample and myocardium was determined.The gene expression of vWF was also quantified.RESULTS:(1)In control group,vWF in blood sample significantly increased(P<0.01).In adenosine treated group,the level of vWF was significantly lower than that in control group(P<0.05).(2)vWF in both infarcted reflow and no-reflow myocardium significantly increased(both P<0.01),while the level of vWF in no-reflow myocardium was significantly higher than that in infarcted reflow myocardium(P<0.01).In adenosine-treated group,the level of vWF in infarcted reflow myocardium was significantly lower than that in control group(P<0.01).(3)The gene expression of vWF in infarcted reflow myocardium significantly up-regulated(P<0.01),while that of vWF in no-reflow myocardium significantly down-regulated(P<0.01).In adenosine-treated group,the level of vWF mRNA in infarcted reflow myocardium was significantly lower than that in control group(P<0.01).CONCLUSION:The endothelium injury is one of the important mechanisms for no-reflow phenomenon.Adenosine prevents endothelium from injury to reduce no-reflow.更多还原