腺苷对猪急性心肌梗死再灌注后vWF的影响  

Effect of adenosine on vWF in the infarcted reflow and no-reflow myocardium of mini-swines

作　　者：赵京林[1] 杨跃进[1] 尤士杰[1] 荆志成[1] 吴永建[1] 杨伟宪[1] 陈纪林[1] 高润林[1] 陈在嘉[1] 

机构地区：[1]中国医学科学院阜外心血管病医院,北京100037

出　　处：《中国病理生理杂志》2006年第9期1669-1673,共5页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助(No.90209038);北京市自然科学基金资助(No.7042044)

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。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 yon 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.

关 键 词：腺苷 von WILLEBRAND因子 心肌梗死 猪 

分 类 号：R363[医药卫生—病理学]