急性心肌梗死大鼠趋化因子表达与心功能的关系  

The relationship between chemokines expression and the cardiac function after acute myocardial infarction in rats

作　　者：葛洪霞[1] 廖玉华[1] 程翔[1] 李彬[1] 

机构地区：[1]华中科技大学同济医学院附属协和医院心内科心血管病研究所,湖北武汉430022

出　　处：《中国病理生理杂志》2006年第5期900-903,共4页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助(No.30370574)

摘　　要：目的:探讨急性心肌梗死(AMI)大鼠心肌局部趋化因子的表达与淋巴细胞浸润及心功能的关系。方法:结扎冠状动脉左前降支建立AMI大鼠模型,实验动物分为3组:心衰组(MI-HF)、未心衰组(MI-NF)和假手术组(sham),假手术组只过线不结扎。于术后3 d、1周、2周检测血流动力学,将左室舒张末期压力(LVEDP)≥15 mmHg者归为心衰组。用半定量RT-PCR方法测定心肌梗死区(包括梗死周边区)趋化因子的mRNA表达,包括γ干扰素诱导的单核因子(MIG)、巨噬细胞炎性蛋白-1α(MIP-1α)、正常T细胞表达和分泌、活化时表达下降的因子(RANTES)。HE染色切片进行梗死区淋巴细胞计数分析。结果:AMI大鼠心肌局部趋化因子的mRNA表达于术后3d开始升高,1周达峰值,且MI-HF组较MI-NF组表达更高(RANTES,0.83±0.05vs0.51±0.19,P<0.05;MIP-1,α1.94±0.30vs1.48±0.33,P<0.05;MIG,1.40±0.27vs0.93±0.28,P<0.05)。RANTES和MIP-1α的表达与淋巴细胞浸润显著相关(RANTES,r=0.35,P<0.05;MIP-1α,r=0.40,P<0.05)。结论:AMI后心肌局部趋化因子RANTES、MIP-1α、MIG表达增高,且趋化因子水平与心功能有相关性,趋化因子可能参与了AMI后心衰的病理生理学发展过程。AIM： Recent studies have identified the importance of inflammation in the development and progression of heart failure. Chemokines are essential factors in the recruitment and activation of leukocytes. They are closely related with inflammation. So the relation between chemokines expression and lymphocytes recruitment and cardiac function after acute myocardial infarction （AMI） was studied. METHODS： Ligating left interventricular branch induced AMI. Experimental rats were divided into three groups： heart failure group （MI-HF）, non- heart failure group （MI- NF） and sham group （sham）. Sham group was made by the same procedure only without ligation. The blood dynamics of rats was examined after 3 days, 1 week and 2 weeks following ligation. Rats, which had a left ventricular end- diastolic pressure （LVEDP） above 15 mmHg, were considered to be in heart failure. Reverse transcription polymerase chain reaction （ RT - PCR） was used to analyze the mRNA expression of chemekines, including monokine induced by IFN - T （MIG）, macrophage inflammatory protein - 1 alpha （ MIP - I a） and regulated upon activation, normal T cell expressed and secreted （RANTES）, in the infarcted region （circumjacent region included）. The numbers of lymphocytes infiltrated in the infarcted region were also counted. RESULTS： MIP-1α, RANTES and MIG mRNA increased at 3 days and reached the peak at 1 week after AMI, significantly higher in MI- HF group than those in MI- NF group （RANTES, 0.83 3±0.05 vs 0.51±0.19, P〈0.05; MIP-1α, 1.94±0.30 vs 1.48±0.33, P〈0.05; MIG, 1.40±0.27 vs 0.93±028, P〈0.05）. The expression of RANTES and MIP-1α were correlated with the infiltration of lymphocytes significantly （RANTES, r =0.35, P 〈0.05; MIP-1α, r =0.40, P 〈0.05）. CONCLUSION： MIG, RANTES and MIP-1α increased in the myocardium after AMI in rats, correlated with cardiac function. The elevation of these chemokines may actively contribute to the pathophysiology of heart failure after AMI.

关 键 词：心肌梗死 炎症趋化因子类 淋巴细胞 心力衰竭 急性心肌梗死 

分 类 号：R542.22[医药卫生—心血管疾病] R363[医药卫生—内科学]