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Cardiovascular Research 1998 38(2):291-300; doi:10.1016/S0008-6363(98)00033-9
© 1998 by European Society of Cardiology
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Copyright © 1998, European Society of Cardiology

A fresh look at reperfusion injury1

H.M. Pipera,*, D. Garcña-Doradob and M. Ovizec

aPhysiologisches Institut, Klinikum der Justus-Liebig-Universität, Aulweg 129, Giessen, Germany
bServicio de Cardiologña, Hospital General Vall d'Hebron, Barcelona, Spain
cHôpital Cardiologique et Pneumologique Louis Pradel, Lyon, France

* Corresponding author. Tel.: +49 (641) 994-7241; Fax: +49 (641) 994-7239.

Received 31 October 1997; accepted 20 January 1998

The first 150 words of the full text of this article appear below.


    1 Introduction
 
In clinical therapy of evolving acute myocardial infarction, coronary reperfusion has proven to be the only way to limit infarct size, provided it occurs soon enough after coronary artery occlusion. However, there is also evidence that reperfusion is accompanied by detrimental manifestations known as ‘reperfusion injury’. Reperfusion injury refers to a causal event associated with reperfusion that had not occurred during the preceding ischemic period and can be entirely attenuated by an intervention given only at the time of reperfusion. It classically includes myocardial stunning, reperfusion arrhythmias and lethal reperfusion injury. Clearly, reperfusion arrhythmias do not represent an important problem for the clinician because their incidence is very low and they can be quite easily treated. Myocardial stunning is usually not a major clinical problem in the context of acute myocardial infarction because it disappears spontaneously and is very sensitive to inotropic agents. Myocardial stunning becomes of serious concern only . . . [Full Text of this Article]


    2 Three initial causes of immediate lethal reperfusion injury
 
2.1 Role of re-energization
2.2 Role of rapid normalization of tissue pH
2.3 Role of rapid normalization of tissue osmolality

    3 Following initial causes: spreading of necrosis
 

    4 The problem of delay of necrosis and initiation of apoptosis
 

    5 Conclusions
 

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