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Salvage of jeopardized myocardium by ischemic preconditioning: is the quest over?

作者信息

Strasser R, Htun P, Schaper W

机构信息

Max-Planck-Institute for Physiological and Clinical Research, Kerckhoff-Klinik, Bad Nauheim, Germany.

出版信息

Mol Cell Biochem. 1996 Jul-Aug;160-161:209-15. doi: 10.1007/BF00240051.

DOI:10.1007/BF00240051
PMID:8901475
Abstract

Helmholtz is quoted to have said that if he'd had any influence in creation he would have returned the human eye to its maker for revisions. The same could be said of the heart with its only very rudimentary ability to defend itself against ischemia. Ischemia was obviously not a problem during evolution: Early man did not live much longer than prime time for reproduction and no selection bias existed to prevent vascular diseases, an affliction of later life. In spite of this natural disadvantage of aged males the number of existing although not very efficient defense mechanisms is surprisingly large. It is the general belief that the knowledge of these mechanisms may lead to the development of new therapies that hopefully improve the imperfect product of natural selection.

摘要

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Adenosine A1 receptors, KATP channels, and ischemic preconditioning in dogs.犬体内的腺苷A1受体、ATP敏感性钾通道与缺血预处理
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短暂缺血或热应激24小时后心脏应激蛋白升高与心肌梗死抗性相关。
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Expression of heat shock proteins in the normal and stunned porcine myocardium.热休克蛋白在正常及顿抑猪心肌中的表达
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Neutral endopeptidase in the heart. Neutral endopeptidase inhibition prevents isoproterenol-induced myocardial hypoperfusion in rats by reducing bradykinin degradation.
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Circulation. 1995 Jan 15;91(2):291-7. doi: 10.1161/01.cir.91.2.291.
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Previous angina alters in-hospital outcome in TIMI 4. A clinical correlate to preconditioning?既往心绞痛对TIMI 4研究中的院内结局有影响。这是一种与预处理相关的临床关联吗?
Circulation. 1995 Jan 1;91(1):37-45. doi: 10.1161/01.cir.91.1.37.
10
The effects of global ischemia and reperfusion on human myocardium: quantitative evaluation by electron microscopic morphometry.全球缺血和再灌注对人体心肌的影响:通过电子显微镜形态计量学进行定量评估。
Ann Thorac Surg. 1982 Feb;33(2):116-22. doi: 10.1016/s0003-4975(10)61895-4.