【摘要】 目的研究人ghrelin对急性心肌梗死(acute myocardial infarction,AMI)致心力衰竭(heart failure,HF)大鼠心肌形态结构变化和心肌细胞凋亡的影响,探索生长素释放肽(growth hormone releasing-peptides,GHRPs)心脏保护活性机制。方法经心电图监测成功永久结扎成年雌性Wistar大鼠左冠状动脉前降支诱导AMI,经B型超声鉴定诱导HF模型成立或穿线不接扎成HF模型对照;以人ghrelin经尾静脉注射进行干预3周;苏木精-伊红(HE)染色观察心肌组织形态结构变化;末端脱氧核苷酰基转移酶介导的d UTP切口末端标记技术分别研究心力衰竭大鼠心肌组织形态、细胞凋亡变化。结果 TUNEL染色结果:永久结扎后心肌细胞排列紊乱,呈颗粒变性,肿胀、核固缩。较多间质纤维化、炎细胞浸润:经人ghrelin干预的的虽有排列紊乱、肿胀和少量颗粒变性外未见典型固缩或严重间质少量纤维化,HF组心肌细胞凋亡指数明显高于ghrelin干预组(P<0.05)。结论外源性ghrelin减少HF大鼠心肌细胞凋亡,抑制心脏重塑而发挥心脏保护活性。更多还原

【Abstract】 Objective To study the effect of human ghrelin on morphosis and cardiomyocytes apoptosis in heart failure(HF) rats derived from acute myocardial infarction(AMI),so as to explore the cardioprotective activity mechanism of growth hormone releasing-peptides(GHRPs).Methods Under the monitoring of the electrocardiogram(ECG) by the multichannel physiological signal collection management system to confirm successfully permanent ligation the left anterior descending coronary artery(LAD) to set up AMI model and then by ultrasound B system to rule out the rats without HF or to make the sham group rats which merely pass through the stylolite beneeth LAD; HF model group rats accept three weeks human ghrelin through tail vein injection,using HE stain technique to analyze the changes of morphosis,the cardiomyocytes apoptosis in HF rats were assessed by terminal deoxynucleotidyl transferase-mediated d UTP nick end labeling(TUNEL).Results TUNEL staining results showed that the cardiomyocytes in rats after permanent LAD ligation aligned extremely irregularly,granular degeneration,swelling,much karyopyknosis and severe interstitial fibrosis,inflammatory cell infiltrate,while in human ghrelin intervention rats,cardiaomyocytes aligned irregularly,swelling and granular degeneration also could be found but without typical karyopyknosis or severe interstitial fibrosis.The cardiomyocytes apoptotic index in HF group rats is significantly higher than that in ghrelin intervention group rats(P < 0.05).Conclusion Extrinsic human ghrelin exerted the cardioprotective activities by reducing the cardiomyocytes apoptosis and inhabitting the cardiac remodeling.更多还原