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缺血预处理

Ischemic preconditioning.

作者信息

Schwarz E R, Whyte W S, Kloner R A

机构信息

Heart Institute Research, Good Samaritan Hospital, Los Angeles, CA 90017-2395, USA.

出版信息

Curr Opin Cardiol. 1997 Sep;12(5):475-81.

PMID:9352175
Abstract

It has been shown that repeated brief coronary occlusions increase myocardial resistance towards prolonged episodes of ischemia. This phenomenon, which renders the heart more tolerant to ischemia with subsequent limitation of infarct size, has been termed ischemic preconditioning and has been described in a variety of species. Preconditioning may also protect the heart against postischemic dysfunction and ventricular arrhythmias. Although the beneficial effects seem to be transient, they re-appear at 24 hours, representing a "second window of protection." Ischemia-induced activation of adenosine receptors and opening of ATP-sensitive potassium channels appear to play a role in the acute cardioprotection. For the late protection, stress protein synthesis may play a role. There is experimental and clinical evidence that preconditioning effects may also exist in the human heart. If so, the mechanisms of ischemic preconditioning might be applied to future therapy.

摘要

已经表明,反复短暂的冠状动脉闭塞会增加心肌对长时间缺血发作的抵抗力。这种现象使心脏对缺血更具耐受性,随后梗死面积受限,被称为缺血预处理,并且已在多种物种中得到描述。预处理还可以保护心脏免受缺血后功能障碍和室性心律失常的影响。尽管有益作用似乎是短暂的,但它们在24小时时会再次出现,代表着“第二个保护窗口”。缺血诱导的腺苷受体激活和ATP敏感性钾通道开放似乎在急性心脏保护中起作用。对于晚期保护,应激蛋白合成可能起作用。有实验和临床证据表明,缺血预处理效应在人类心脏中可能也存在。如果是这样,缺血预处理的机制可能会应用于未来的治疗。

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Ischemic preconditioning.缺血预处理
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引用本文的文献

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Biomed Res Int. 2019 Apr 16;2019:6592464. doi: 10.1155/2019/6592464. eCollection 2019.
2
Protective role of the deSUMOylating enzyme SENP3 in myocardial ischemia-reperfusion injury.去 SUMO 化酶 SENP3 在心肌缺血再灌注损伤中的保护作用。
PLoS One. 2019 Apr 11;14(4):e0213331. doi: 10.1371/journal.pone.0213331. eCollection 2019.
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The role of mitochondria in protection of the heart by preconditioning.
线粒体在预处理对心脏的保护作用中的角色。
Biochim Biophys Acta. 2007 Aug;1767(8):1007-31. doi: 10.1016/j.bbabio.2007.05.008. Epub 2007 Jun 2.
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Protective effect of nitric oxide induced by ischemic preconditioning on reperfusion injury of rat liver graft.缺血预处理诱导的一氧化氮对大鼠肝移植再灌注损伤的保护作用。
World J Gastroenterol. 2004 Jan;10(1):73-6. doi: 10.3748/wjg.v10.i1.73.
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Ischaemic preconditioning inhibits opening of mitochondrial permeability transition pores in the reperfused rat heart.缺血预处理可抑制再灌注大鼠心脏线粒体通透性转换孔的开放。
J Physiol. 2003 Jun 1;549(Pt 2):513-24. doi: 10.1113/jphysiol.2003.034231. Epub 2003 Apr 11.
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The effects of ischaemic preconditioning, diazoxide and 5-hydroxydecanoate on rat heart mitochondrial volume and respiration.缺血预处理、二氮嗪和5-羟基癸酸对大鼠心脏线粒体体积和呼吸的影响。
J Physiol. 2002 Dec 15;545(3):961-74. doi: 10.1113/jphysiol.2002.031484.
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Preservation of mitochondrial function by diazoxide during sustained ischaemia in the rat heart.二氮嗪在大鼠心脏持续性缺血期间对线粒体功能的保护作用。
Br J Pharmacol. 2000 Mar;129(6):1219-27. doi: 10.1038/sj.bjp.0703148.