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Cardiovascular Research 2000 48(2):185-187; doi:10.1016/S0008-6363(00)00213-3
© 2000 by European Society of Cardiology
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Copyright © 2000, European Society of Cardiology

Reperfusion injury and ischemic preconditioning: two sides of a coin?

Jan W.T Fiolet*

Experimental and Molecular Cardiology Group, Department of Experimental Cardiology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE, Amsterdam, The Netherlands

* Tel.: +31-20-566-3265; fax: +31-20-697-5458 j.w.fiolet@amc.uva.nl

Received 30 August 2000; accepted 30 August 2000

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

See article by Xiao and Allen [1] (pages 244–253) in this issue.


   1 Introduction
 
A substantial body of presently available evidence supports the contention that cytosolic accumulation of sodium during ischemia is instrumental to the elevation of intracellular calcium during ischemia and reperfusion through prolonged reversed mode operation of the Na+/Ca2+-exchanger [1–10], which eventually leads to irreversible injury. The study by Xiao and Allen [1] published in this issue of Cardiovascular Research further elaborates on the original hypothesis by Lazdunski et al. [2] and previous work of the authors [11] that the Na+/H+-exchanger is pivotal in causing myocardial reperfusion injury following prolonged ischemia and adds to the ongoing debate on the subject. The study provides experimental evidence that the Na+/H+-exchanger is relatively inactive during ischemia, but rapidly re-activates early during reperfusion causing an increase in cytosolic . . . [Full Text of this Article]


   2 [Na]i, reperfusion injury and preconditioning
 

   3 Thermodynamic considerations
 

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