摘要
目的:观察腺苷(Ado)对大鼠心肌缺血再灌注损伤(MIRI)的保护作用,探讨其可能的作用机制。方法:健康Wistar大鼠36只,随机分成3组。假手术组:只穿线不结扎冠状动脉;腺苷组:于结扎前1min给予Ado(0.4ml/kg)左心室内注入;对照组:给予等量生理盐水左心室内注入。开胸结扎左冠状动脉前降支30min,再灌注45min,制作大鼠MIRI模型。实验结束后检测心肌组织超氧化物歧化酶(SOD)、丙二醛(MDA)含量;测量缺血前与再灌注45min后左心室收缩期峰压(LVSP)差值和左心室舒张期末压(LVEDP);HE染色观察心肌组织形态结构。结果:与对照组比较,腺苷组大鼠SOD活力提高(P<0.05)而MDA生成量减少(P<0.01),且LVSP差值及LVEDP均减小(P<0.05,P<0.01);与假手术组比较,对照组大鼠心肌组织SOD活力明显下降(P<0.05)而MDA生成量明显增高(P<0.01),且LVSP差值及LVEDP明显增高(P<0.05,P<0.01);对照组大鼠心肌纤维断裂坏死,大量炎性细胞浸润,而腺苷组无出血、坏死,有少量炎性细胞浸润。结论:心肌缺血再灌注可导致缺血心肌进一步损伤,Ado可通过抑制氧自由基的产生,减少炎性细胞的浸润,对缺血再灌注损伤心肌有保护作用。
Objective： To observe the protective effect of adenosine pretreatment in the rat model of myocardial ischemia-reperfusion injury （MIRI） and the possible mechanism. Methods： Thirty-six healthy Wistar rats were randomly divided into sham operation group,adenosine group, and control group. The left anterior descending coronary arteries （LADs） of rats were not ligated in sham operation group. In adenosine and control groups,the rat model of MIRI was established by ligating the LADs for 30 minutes and then performing reperfusion for 45 minutes. The rats were infused with 0.4 ml/kg of adenosine into left ventricles in adenosine group and equal quantity of normal saline in control group before hgafing the LADs. The activity of superoxide dismutase （SOD） and the content of malonaldehyde （MDA） in the left ventricles were determined. The difference in left ventricular systolic pressure （LVSP） and the left ventricular end-diastolic pressure （LVEDP） before ischemia and 45 minutes after reperfusion were determined. The morphological changes of myocardium were observed after HE staining. Results： Compared with control group,in adenosine group,the activity of SOD significantly increased （P 〈 0.05）,and the content of MDA, the difference in LVSP,and LVEDP significantly decreased （P 〈 0.01 ,P 〈 0.05,P〈0.01 ）. Compared with sham operation group,in control group,the activity of SOD significantly decreased （P 〈 0.05 ）,and the content of MDA,the difference in LVSP,and LVEDP significantly increased （P 〈 0.01,P 〈 0.05,P 〈 0.01）. Myocardial fiber necrosis and inflammatory cell infiltration were found in control group,but in adenosine group there was no necrosis and relatively little inflammatory cell infiltration. Conclusion： Adenosine could prevent MIRI in rats by inhibiting the production of oxygen free radicals and reducing inflammatory cell infiltration.
出处
《中国医科大学学报》
CAS
CSCD
北大核心
2007年第2期145-147,共3页
Journal of China Medical University
关键词
心肌缺血再灌注损伤
腺苷
保护作用
myocardial ischemia reperfusion injury
adenosine
protective effect
作者简介
王阳（1975-），女，主治医师，硕士．
Corresponding Author＇s E-mail. qigx2002@medmail.com.cn
