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当前关于心肌再灌注和再灌注损伤的研究观点。

Current research views on myocardial reperfusion and reperfusion injury.

作者信息

Yellon D M, Downey J M

机构信息

Department of Cardiology, University College Hospital, London, UK.

出版信息

Cardioscience. 1990 Jun;1(2):89-98.

PMID:2102803
Abstract

This article discusses the types of reperfusion injury, some of the causes of the injury and the possible role of the radical scavengers in protecting against it. The methodological problems that have plagued this field are explored and some answers put forward, although we are sure that further questions will have been raised. There are now reasons to question the use of the tetrazolium staining procedure which has become the "gold standard" for measurements of infarct size. It seems likely that it is adequate only as a screening procedure, and even then will be associated with a troublesome number of false positives. Collateral flow is an important determinant of infarct size and simultaneous measurements of collateral flow are essential in the interpretation of the effects of drugs on infarct size. The limitations of the various animal models are important when relating experimental findings to the clinical condition. After a decade of research, reperfusion injury is itself still under question, and there remains confusion as to the role that oxygen-derived free radicals may play in the ischemic/reperfused myocardium. However, we believe that, from the experimental data available, oxygen derived free radicals are involved in the overall pathophysiology of ischemia and reperfusion, although the full extent remains to be clarified and the therapeutic implications explored.

摘要

本文讨论了再灌注损伤的类型、损伤的一些原因以及自由基清除剂在预防再灌注损伤中可能发挥的作用。文中探讨了困扰该领域的方法学问题,并给出了一些答案,尽管我们确信还会引发更多问题。目前有理由质疑已成为测量梗死面积“金标准”的四氮唑染色法。它似乎仅适用于筛查,即便如此,也会出现大量令人头疼的假阳性结果。侧支血流是梗死面积的重要决定因素,在解释药物对梗死面积的影响时,同时测量侧支血流至关重要。在将实验结果与临床情况相关联时,各种动物模型的局限性很重要。经过十年的研究,再灌注损伤本身仍存在疑问,关于氧自由基在缺血/再灌注心肌中可能发挥的作用也仍存在困惑。然而,我们认为,从现有实验数据来看,氧自由基参与了缺血和再灌注的整体病理生理学过程,尽管其全部影响仍有待阐明,治疗意义也有待探索。

相似文献

1
Current research views on myocardial reperfusion and reperfusion injury.当前关于心肌再灌注和再灌注损伤的研究观点。
Cardioscience. 1990 Jun;1(2):89-98.
2
Superoxide dismutase plus catalase therapy delays neither cell death nor the loss of the TTC reaction in experimental myocardial infarction in dogs.超氧化物歧化酶加过氧化氢酶疗法并不能延缓犬实验性心肌梗死中的细胞死亡及三苯基氯化四氮唑反应的丧失。
J Mol Cell Cardiol. 1993 Apr;25(4):367-78. doi: 10.1006/jmcc.1993.1043.
3
Free radicals and myocardial ischemia and reperfusion injury.自由基与心肌缺血再灌注损伤
J Lab Clin Med. 1987 Jul;110(1):13-30.
4
Free radical scavengers in myocardial ischemia.心肌缺血中的自由基清除剂。
Fed Proc. 1987 May 15;46(7):2413-21.
5
Oxidative damage to the myocardium: a fundamental mechanism of myocardial injury.心肌的氧化损伤:心肌损伤的一种基本机制。
Cardioscience. 1991 Dec;2(4):199-216.
6
Effects of oxygen free radicals and scavengers on the cardiac extracellular collagen matrix during ischemia-reperfusion.氧自由基及清除剂对缺血再灌注期间心脏细胞外胶原基质的影响。
Can J Cardiol. 1994 Mar;10(2):203-13.
7
[Reperfusion and postconditioning in acute ST segment elevation myocardial infarction. A new paradigm for the treatment of acute myocardial infarction. From bench to bedside?].[急性ST段抬高型心肌梗死的再灌注与后适应。急性心肌梗死治疗的新范例。从实验台到病床边?]
Arch Cardiol Mex. 2006 Oct-Dec;76 Suppl 4:S76-101.
8
Evaluation of free radical injury in myocardium.
Toxicol Pathol. 1990;18(4 Pt 1):470-80.
9
Prevention of myocardial reperfusion injury with free radical scavengers. An experimental study.自由基清除剂预防心肌再灌注损伤的实验研究
Chin Med J (Engl). 1989 Oct;102(10):768-73.
10
Cardiac performance during reperfusion improved by pretreatment with oxygen free-radical scavengers.再灌注期间的心脏功能通过用氧自由基清除剂预处理得到改善。
J Thorac Cardiovasc Surg. 1986 Feb;91(2):290-5.

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Protecting the ischaemic and reperfused myocardium in acute myocardial infarction: distant dream or near reality?保护急性心肌梗死中的缺血及再灌注心肌:遥不可及的梦想还是近在咫尺的现实?
Heart. 2000 Apr;83(4):381-7. doi: 10.1136/heart.83.4.381.
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Reperfusion Injury: Basic Concepts and Protection Strategies.
再灌注损伤:基本概念与保护策略
J Thromb Thrombolysis. 1997 Jan;4(1):7-24. doi: 10.1023/a:1017569611074.
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Hsp70 in myocardial ischaemia.心肌缺血中的热休克蛋白70
Experientia. 1994 Nov 30;50(11-12):1075-84. doi: 10.1007/BF01923464.
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Overexpression of the rat inducible 70-kD heat stress protein in a transgenic mouse increases the resistance of the heart to ischemic injury.大鼠诱导型70kD热应激蛋白在转基因小鼠中的过表达增强了心脏对缺血性损伤的抵抗力。
J Clin Invest. 1995 Apr;95(4):1446-56. doi: 10.1172/JCI117815.
6
Comparison of triphenyltetrazolium chloride (TTC) staining versus detection of fibronectin in experimental myocardial infarction.实验性心肌梗死中氯化三苯基四氮唑(TTC)染色与纤连蛋白检测的比较
Histochemistry. 1993 Apr;99(4):265-75. doi: 10.1007/BF00269099.
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Basic fibroblast growth factor is cardioprotective in ischemia-reperfusion injury.碱性成纤维细胞生长因子对缺血再灌注损伤具有心脏保护作用。
Mol Cell Biochem. 1995 Feb 23;143(2):129-35. doi: 10.1007/BF01816946.
8
Enzyme and immunohistochemical assessment of myocardial damage after ischaemia and reperfusion in a closed-chest pig model.在闭胸猪模型中对缺血再灌注后心肌损伤进行酶学和免疫组织化学评估。
Histochemistry. 1992 Dec;98(6):341-53. doi: 10.1007/BF00271069.