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心肌早期缺血再灌流损伤HSP_(70)的表达

Expression of HSP_(70) in Early Myocardial Ischemia and Reperfusion Injury
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摘要 目的 探讨早期缺血再灌流损伤心肌组织热休克蛋白 70 (HSP70 )的变化 ,为心源性猝死的法医病理学鉴定寻找新的依据。方法 建立家兔早期心肌缺血再灌流动物模型 ,用免疫组化SABC法观察HSP70 的表达。结果 心肌缺血 15min再灌流 30min后 ,再灌流区心内膜下可见HSP70 阳性表达 ;缺血 30min再灌流 30min后 ,HSP70 阳性反应细胞数目较多 ,散布于心肌全层 ;缺血 6 0min再灌流 30min后 ,再灌流区阳性表达明显减少 ,而其边缘见阳性表达略有增强。各实验组正常区和对照组心肌组织均未见阳性反应。结论 心肌组织HSP70 的阳性表达是一项显示心肌早期缺血再灌流损伤的灵敏指标 ,HSP70 的免疫组化检测对缺血再灌流损伤所致心性猝死的死后诊断具有一定的应用价值。 Objective To study the changes of the expression of HSP-{70} in myocardial tissue after early myocardial ischemia and reperfusion injury(MI/R),searching for a new evidence for forensic pathological diagnosis of sudden cardiac death. Methods The rabbit model of MI/R was established, immunohistochemical SABC method was used to observe the expression of HSP-{70} in myocardial tissue. Results The expression of HSP-{70} could be detected in the subendothalial area of MI/R after 15min ischemia followed by 30min reperfusion,and the positive reaction cells of HSP-{70} diffused in all myocardial tissue of MI/R after 30 min ischemia and 30 min reperfusion.The positive expression decreased in the area of MI/R but slightly increased in its margin area after 60 min ischemia followed by 30 min reperfusion.The myocardium in the control group and nonischemic area of the experimental groups showed negative staining. Conclusion The positive expression of HSP-{70} in myocardial tissue is a sensitive index to reveal MI/R,and immunohistochemical detection of HSP-{70} could be helpful to the postmortem diagnosis of sudden cardiac death caused by MI/R.
出处 《皖南医学院学报》 CAS 2002年第2期128-130,共3页 Journal of Wannan Medical College
关键词 缺血再灌流损伤 热休克蛋白70 免疫组织化学 ischemia and reperfusion injury HSP-{70} Immunohistochemistry
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  • 1[1]Myerburg RJ, Kessler KM, Mallon SM, et al. Life-threatening ventricular arrhythmias in patients with silent myocardial ischemia due to coronary-artery spasm. N Engl J Med ,1992; 326(22):1451~455
  • 2[2]Nappo A, Varesic C, Rossi L, et al. Sudden cardiac death in non-professional athletes. Pathologica ,1997 ; 89(5):517~522
  • 3[3]Fberhardt F, Mehlhorn K, Larose K, et al. Structural myocardial changes after coronary artery surgery. Eur J Cli Invest, 2000 ; 30(11): 938~946
  • 4[4]Corr PB, Witkowski FX. Potential electrophysicologic mechanisms responsible for dysrhythmias associated with reperfusion of ischemic myocardium. Circulation, 1983 ;68(2 Pt2):16~24
  • 5[5]Kita T. The role of heat shock proteins on the disordered tissues:implication for the pathogenesis and diagnostics in the forensic practice. Nippon Hoigaku Zasshi, 2000;54(3):367~71
  • 6[6]Dapunt OE, Raji MR, Jeschkeit S, et al. Intracoronary shunt insertion prevents myocardial stunning in a juvenile porcine MIDCAB model absent of coronary artery disease. Eur J Cardiothorac Surg , 1999 ; 15(2):173~179
  • 7[7]Taggart DP, Bakkenist CJ, Biddolph SC, et al. Induction of myocardial heat shock protein 70 during cardiac surgery. J Pathol, 1997 ;182(3):362~366
  • 8[8]Fberhardt F, Mehlhorn K, Larose K, et al. Structural myocardial changes after coronary artery surgery. Eur J Cli Invest, 2000 ; 30(11): 938~946
  • 9[9]Itoh S, Yanagishita T, Mukae S, et al. Study on reperfusion injury on sarcopcasmic reticulum in acute myocardial ischemia. Jpn Circ J, 1992 ;56(4):381~391
  • 10[10]Ibba Manneschi L, Formigli L, Taoni A, et al. Ultrastructural evidence of myocardial alterations in the course of heterotopic heart transplantation. J Submicrosc Cytol Pathol, 1996 ; 28(3):401~418

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