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Cardiovascular Research 2000 45(4):810-812; doi:10.1016/S0008-6363(99)00420-4
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Ischemia–reperfusion associated myocardial contractile dysfunction may depend on Ca2+-activated cytoskeleton protein degradation

L Rappaport*

Unité 127 INSERM, IFR ‘Circulation’, D. Diderot University, Lariboisière Hospital, 41 bd. de l’Hôpital, Paris 75475, France

* Tel.: +33-1-44-6317-40/21; fax: +33-1-4874-2315

Received 9 December 1999; accepted 9 December 1999

The first 10% of the full text of this article appears below.

See article by Papp et al. [9] (pages 981–993) in this issue.


   1 Introduction
 
Postischemic dysfunction, or myocardial stunning, is defined as ‘the mechanical dysfunction that persists after reperfusion despite the absence of irreversible damage and restoration of normal or near normal coronary flow’ (for a review, see Ref. [1]). Myocardial stunning may be considered as a relatively mild, sublethal injury that must be distinguished from myocardial infarction. It is generally admitted that myocardial stunning is a multifactorial process, that mostly depends on two major mechanisms: (1) generation of oxygen radicals, (2) calcium overload, both being probably involved in the process (for review, see Ref. [1]).

The calcium hypothesis may explain many key features of the stunned myocardium. It has been postulated that calcium overload during reflow triggers myofilament dysfunction which uncouples excitation from contraction, so that for any given calcium transient, the myocardium generates less force [2].

. . . [Full Text of this Article]


   2 Proteolytic activity of calpain on cytoskeletal proteins
 

   3 Desmin
 

   4 Myofibrillar dysfunction may also depend on a Ca2+ dependent binding of soluble proteins to the myofibrils
 

   5 Conclusion
 

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