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Cardiovascular Research 2001 50(1):164-166; doi:10.1016/S0008-6363(01)00229-2
© 2001 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Na+ entry during ischemia, reperfusion and preconditioning

David G Allen* and Xiao-hui Xiao

Department of Physiology and Institute for Biomedical Research, University of Sydney F13, NSW 2006, Australia

* Corresponding author. Tel.: +61-2-9351-4602; fax: +61-2-9351-4602

Received 23 January 2001; accepted 23 January 2001

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

In our recent series of papers [1–3] we have measured intracellular sodium and pH ([Na+]i and pHi) in rat hearts during ischemia and reperfusion and draw the following conclusions about the activity of the cardiac Na+/H+ exchanger (NHE1). (i) NHE1 is inactive during ischemia. (ii) Normally NHE1 reactivates rapidly on reperfusion causing a large Na+ influx which is the precursor to much of the cellular damage. (iii) However in the preconditioned heart NHE1 remains inactive during early reperfusion and this underlies much of the protective effects of preconditioning. Our evidence and interpretation are different to many earlier studies, as Avkiran et al. [4] point out, and we are pleased to have this opportunity to debate the reasons for these differences and consider the implications of our novel interpretation.

We would first like to comment on the statement by Avkiran et al. ‘Much of this evidence, which suggests . . . [Full Text of this Article]


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 Cardiovasc ResHome page
D. G Allen and X.-H. Xiao
Role of the cardiac Na+/H+ exchanger during ischemia and reperfusion
Cardiovasc Res, March 15, 2003; 57(4): 934 - 941.
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