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Cardiovascular Research 2001 49(4):693-694; doi:10.1016/S0008-6363(01)00189-4
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Adenosine as an important mediator of post-ischaemic neuronal stunning

John Pernow*

Department of Cardiology, Karolinska Hospital, S-171 76 Stockholm, Sweden

* Tel.: +46-8-5177-5876; fax: +46-8-311-044 john.pernow@ks.se

Received 19 December 2000; accepted 28 December 2000

KEYWORDS Adenosine; Ischaemia; Stunning

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

See article by Burgdorf et al. [11] (pages 713–720) in this issue.

A brief period of ischaemia is known to induce a prolonged period of reversible myocardial dysfunction despite normalized electrocardiogram and absence of histological signs of necrosis. This was first described by Heyndrickx and co-workers [1] who found that myocardial function was depressed for several hours following a 15-min period of coronary artery occlusion in dogs. Braunwald and Kloner [2] subsequently named this phenomenon ‘myocardial stunning’. Although the exact mechanism underlying myocardial stunning is not fully understood, results from several studies indicate that it can be mediated by increased myocyte calcium levels and oxygen-derived free radicals during ischaemia and the initial part of . . . [Full Text of this Article]


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