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目的评价急性心肌梗死(AMI)再灌注后内皮素-1(ET-1)的变化及腺苷对ET-1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。采用放射免疫方法测定AMI前5min、AMI后5min、AMI后180min和再灌注后5min和60min血浆ET-1的含量及正常、缺血、无再流区心肌组织ET-1的变化;逆转录-聚合酶链反应的方法观察正常、缺血和无再流区心肌组织ET-1mRNA的表达。结果与AMI前比较,对照组和腺苷组AMI后5min、AMI后180min、再灌注后5min和60min的血清ET-1水平均显著升高(P<0·01),且呈递增趋势(P<0·01)。腺苷组除AMI前外,各时间点的血浆ET-1水平均显著低于对照组(P<0·05,P<0·01)。与正常区心肌组织比较,对照组和腺苷组缺血区和无再流区心肌组织ET-1含量均显著升高(P<0·01),且无再流区ET-1含量升高比缺血区更显著(P<0·01)。与对照组比较,腺苷组仅缺血区心肌组织ET-1含量显著降低(P<0·01)。与正常区心肌组织比较,对照组和腺苷组缺血区心肌组织ET-1的mRNA表达均显著上调(P<0·01),而无再流区心肌组织ET-1的mRNA表达均显著下降(P<0·01)。与对照组比较,腺苷组仅在缺血区ET-1的mRNA表达显著降低(P<0·01)。结论内皮细胞受损可能是无再流发生的重要机制之一,腺苷可能通过保护内皮细胞起到减少无再流的作用。
Objective To evaluate the changes of endothelin-1 (ET-1) and the effect of adenosine on ET-1 after acute myocardial infarction (AMI) reperfusion in rats and to explore the possible mechanism of no-reflow. Methods Twenty-four Chinese miniature pigs were randomly divided into control group, adenosine group and sham operation group, with 8 in each group. Coronary artery ligation 3h, release 1h prepared AMI reperfusion model. Radioimmunoassay was used to determine the plasma levels of ET-1 at 5 min before AMI, 5 min after AMI, 180 min after AMI, 5 min and 60 min after reperfusion, and the changes of ET-1 in normal, ischemic and non-reflow myocardium. Polymerase chain reaction method was used to observe the expression of ET-1mRNA in normal, ischemic and non-reflow myocardium. Results Compared with those before AMI, ET-1 levels in control group and adenosine group were significantly increased at 5 min after AMI, 180 min after AMI, 5 min and 60 min after reperfusion (P <0.01), and showed an increasing trend (P <0 · 01). In addition to AMI, adenosine group plasma ET-1 levels were significantly lower than the control group (P <0.05, P <0.01). Compared with normal myocardium, the content of ET-1 in myocardium of ischemic area and no-reflow area of control group and adenosine group were significantly increased (P <0.01), and there was no increase of ET-1 in reflowed area More significantly than the ischemic area (P <0.01). Compared with the control group, the content of ET-1 in the adenosine group was significantly decreased only in the ischemic myocardium (P <0.01). Compared with the normal myocardium, the mRNA expression of ET-1 in the ischemic myocardium of control group and adenosine group was significantly increased (P <0.01), while the mRNA expression of ET-1 in the non-reflow myocardium was significantly increased Decreased (P <0.01). Compared with the control group, the expression of ET-1 mRNA in adenosine group was significantly decreased only in ischemic area (P <0.01). Conclusions Endothelial cell damage may be one of the important mechanisms of no-reflow. Adenosine may play a role in reducing no-reflow by protecting endothelial cells.