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Cardiovascular Research 2002 53(2):286-289; doi:10.1016/S0008-6363(01)00550-8
© 2002 by European Society of Cardiology
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Copyright © 2001, European Society of Cardiology

Does adenosine protect the heart by acting on the sarcoplasmic reticulum?

Kanigula Mubagwa*

Centre for Experimental Surgery and Anaesthesiology, University of Leuven, Campus Gasthuisberg, Herestraat 49, Leuven, B-3000 Belgium

kanigula.mubagwa@med.kuleuven.ac.be

* Tel.: +32-16-347-132; fax: +32-16-347-139

Received 27 November 2001; accepted 27 November 2001

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

See article by Zucchi et al. [9] (pages 326–333) in this issue.


   1. Altered ion homeostasis during ischemia: critical role of intracellular Ca2+ overload
 
Ischemic heart diseases still constitute the leading cause of mortality and morbidity in industrialized countries; hence a great deal of research is devoted at understanding the underlying mechanisms and at finding means to prevent, delay or attenuate ischemic injury. Intracellular ion homeostasis is altered during ischemia, with the concentrations of H+, Na+, Mg2+, Ca2+ and phosphate increasing markedly (see Ref. [1]). This disturbance of cellular homeostasis, especially the intracellular Ca2+ (Cai) overload, is considered to play a key role in the cell damage during ischemia and reperfusion, and procedures that reduce the Cai rise do protect the myocardium by attenuating or delaying ischemic/reperfusion injury. The increased Cai is supposed to cause cell damage by activating excessive ATP utilization as well as lipolytic and proteolytic enzymes. How the Cai overload is brought about is . . . [Full Text of this Article]


   2. Ischemic preconditioning and the role of adenosine
 

   3. Is an altered SR function the mechanism underlying protection by ischemic preconditioning?
 

   4. Does adenosine alter the SR function?
 

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