AJP - Heart Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Heart Circ Physiol 284: H798-H803, 2003; doi:10.1152/ajpheart.00659.2002
0363-6135/03 $5.00
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via ISI Web of Science (11)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Haist, J. V.
Right arrow Articles by Karmazyn, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Haist, J. V.
Right arrow Articles by Karmazyn, M.
Vol. 284, Issue 3, H798-H803, March 2003

Effective protection by NHE-1 inhibition in ischemic and reperfused heart under preconditioning blockade

James V. Haist, Claire N. Hirst, and Morris Karmazyn

Department of Physiology and Pharmacology, University of Western Ontario, London, Ontario, Canada N6A 5C1

We compared the protective effects of ischemic preconditioning (IPC) and the Na+/H+ exchanger-1 (NHE-1) inhibitor cariporide in isolated rat hearts subjected to global ischemia (45 or 90 min) and 30-min reperfusion and determined the protective effects of cariporide under IPC blockade with the mitochondrial ATP-sensitive K+ channel blocker 5-hydroxydecanoate (5-HD). With 45-min ischemia, both IPC and cariporide equally increased maximum recovery of left ventricular developed pressure twofold (P < 0.05), although recovery was significantly greater with cariporide for the first 15 min of reperfusion. 5-HD almost completely blocked the protective effects of IPC on recovery but had no influence on the salutary effects of cariporide. With 90-min ischemic control, recovery was only 3% of preischemia and was unaffected by IPC, although cariporide increased recovery to ~30% (P < 0.05). This was associated with a 37% preservation of viable cardiac cells, whereas no structurally intact cells were found in either IPC or control hearts. Our study shows that NHE-1 inhibition is a more effective cardioprotective strategy than IPC in this model, possibly because of enhanced myocyte salvage, and because protection by NHE-1 inhibition is completely unaffected by IPC blockade with 5-HD.

sodium-hydrogen exchange; cariporide; cardioprotection


This article has been cited by other articles:


Home page
 Cardiovasc ResHome page
S. Javadov, A. Choi, V. Rajapurohitam, A. Zeidan, A. G. Basnakian, and M. Karmazyn
NHE-1 inhibition-induced cardioprotection against ischaemia/reperfusion is associated with attenuation of the mitochondrial permeability transition
Cardiovasc Res, January 15, 2008; 77(2): 416 - 424.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Physiol. Heart Circ. Physiol.Home page
B. C. Blunt, Y. Chen, J. D. Potter, and P. A. Hofmann
Modest actomyosin energy conservation increases myocardial postischemic function
Am J Physiol Heart Circ Physiol, March 1, 2005; 288(3): H1088 - H1096.
[Abstract] [Full Text] [PDF]

Home page
 CirculationHome page
Y. Teshima, M. Akao, S. P. Jones, and E. Marban
Cariporide (HOE642), a Selective Na+-H+ Exchange Inhibitor, Inhibits the Mitochondrial Death Pathway
Circulation, November 4, 2003; 108(18): 2275 - 2281.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online