期刊文献+

大鼠急性心肌梗死后的心肌细胞凋亡 被引量:10

Cardiomyocyte apoptosis after acute myocardial infarction in rats
暂未订购
导出
摘要 目的:研究大鼠急性心肌梗死(acutemyocardialinfarction,AMI)后心肌细胞凋亡的发生情况。方法:实验选用105只雌性SD大鼠,随机抽取78只以结扎左冠状动脉前降支的方法制备AMI模型,术后24h存活的43只作为心肌梗死组;另设假手术组(n=27);各组再按观察时点随机分为48h和4周两亚组,即:心肌梗死48h(n=11)和心肌梗死4周(n=13)组,假手术48h(n=10)和假手术4周(n=10)组。末端脱氧核糖核酸转移酶介导的dUTP切口末端标记技术(TUNEL)和DNA凝胶电泳检测心肌细胞凋亡。结果:AMI大鼠梗死区心肌细胞坏死和瘢痕形成的同时,梗死/瘢痕区、梗死边缘区和非梗死区的心肌细胞凋亡指数均显著升高犤心肌梗死48h组分别为(212.86±155.75)/1000,(198.16±120.0)/1000和(63.23±45.43)/1000,心肌梗死4周组分别为(235.14±130.43)/1000,(80.33±44.29)/1000和(31.61±16.39)/1000,P<0.05~0.01犦。结论:大鼠发生AMI后,梗死区心肌细胞坏死和瘢痕形成的同时,梗死/瘢痕区、梗死边缘区和非梗死区均有心肌细胞发生凋亡。 AIM:To investigate cardiomyocyte apoptosis after acute myocardial infarction(AMI) in rats.<METHODS:AMI model was established with the ligation of anterior descending branch of left coronary artery in 78 randomly selected from 105 female SD rats.Twenty four hours after operation,the 43 survivors were served as AMI group.Another 27 rats was selected randomly as sham operation group.The each group was randomly reassigned to 48 hour and 4 week subgroups according to the observation time,that was:48 hour AMI(n=11) and 4 week AMI(n=13) subgroups,48 hour sham operation(n=10) and 4 week sham operation(n=10) subgroups.Cardiomyocyte apoptosis was detected with in situ terminal deoxynucleotidyl transferase(TdT) mediated dUTP nick end labeling(TUNEL) and DNA gel electrophoresis.<RESULTS:Along with cardiomyocyte necrosis and scar formation in the infracted area in AMI rats,cardiomyocyte apoptosis index was significantly increased in the infracted/scar,border and non infarcted areas[(212.86 ± 155.75)/1 000,(198.16± 120.0)/1 000 and (63.23± 45.43)/ 1 000 in 48 hour AMI subgroup,(235.14± 130.43)/1 000,(80.33 ± 44.29)/1 000 and (31.61± 16.39)/1 000 in 24 week AMI subgroup,P< 0.05- 0.01].<CONCLUSION:After AMI in rats,cardiomyocyte apoptosis occur in the infarction/scar,border and non infarcted areas along with cardiomyocyte necrosis and scar formation in the infarcted areas.
出处 《中国临床康复》 CSCD 2004年第36期8202-8203,共2页 Chinese Journal of Clinical Rehabilitation
  • 相关文献

参考文献8

  • 1Narula J, Haider N, Virmani R, et al. Apoptosis in myocytes in end - stage heart failure. N Engl J Med 1996:335(16): 1182-9
  • 2livetti G, Abbi R, Quaini F, et al. Apoptosis in the failing human heart. N Engl J Med 1997; 336 (16): 1131 - 41
  • 3Weisman HF BD, Mannisi JA, Weisfeldt ML, et al. Cellular mechanisms of myocardial infarct expansion. Circulation 1988; 78 ( 1 ): 186 - 201
  • 4Pfeffer JM, Pfeffer MA, Braunwald E. Influence of chronic captopril therapy on the infarcted left ventricle of the rat. Circ Res 1985; 57 ( 1 ): 84 - 95
  • 5Yang YJ, Tang YD, Ruan YM, et al. Comparative effects of carvedilol and losartan alone and in combination for preventing left ventricular remodeling after acute myocardial infarction in rats. Circ J 2003; 67 (2): 159 -62
  • 6Cheng W, Kajstura J, Nitahara JA, et al. Programmed myocyte cell death affects the viable myocardium after infarction in rats. Exp Cell Res 1996; 226(2): 316 -27
  • 7Bialik S, Geenen DL, Sasson IE, et al. Myocyte apoptosis during acute myocardial infarction in the mouse localizes to hypoxic regions but occurs independently of p53. J Clin Invest 1997; 100(6): 1363 -72
  • 8Kajstura J, Cheng W, Reiss K, et al. Apoptotic and necrotic myocyte cell deaths are independent contributing variables of infarct size in rats. Lab Invest 1996; 74(1):86-107

同被引文献115

引证文献10

二级引证文献39

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部