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Publication Details
AFRICAN RESEARCH NEXUS
SHINING A SPOTLIGHT ON AFRICAN RESEARCH
biochemistry, genetics and molecular biology
Lovastatin interferes with the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts
American Journal of Physiology - Heart and Circulatory Physiology, Volume 294, No. 5, Year 2008
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Description
Statins have been shown to be cardioprotective; however, their interaction with endogenous cardioprotection by ischemic preconditioning and postconditioning is not known. In the present study, we examined if acute and chronic administration of the 3-hydroxy-3-methylglutaryl CoA reductase inhibitor lovastatin affected the infarct size-limiting effect of ischemic preconditioning and postconditioning in rat hearts. Wistar rats were randomly assigned to the following three groups: 1) vehicle (1% methylcellulose per os for 12 days), 2) chronic lovastatin (15 mg·kg -1·day-1 per os for 12 days), and 3) acute lovastatin (1% methylcellulose per os for 12 days and 50 μmol/l lovastatin in the perfusate). Hearts isolated from the three groups were either subjected to a nonconditioning (aerobic perfusion followed by 30-min coronary occlusion and 120-min reperfusion, i.e., test ischemia-reperfusion), preconditioning (three intermittent periods of 5-min ischemia-reperfusion cycles before test ischemia-reperfusion), or postconditioning (six cycles of 10-s ischemia-reperfusion after test ischemia) perfusion protocol. Preconditioning and postconditioning significantly decreased infarct size in vehicle-treated hearts. However, preconditioning failed to decrease infarct size in acute lovastatin-treated hearts, but the effect of postconditioning remained unchanged. Chronic lovastatin treatment abolished postconditioning but not preconditioning; however, it decreased infarct size in the nonconditioned group. Myocardial levels of coenzyme Q9 were decreased in both acute and chronic lovastatin-treated rats. Western blot analysis revealed that both acute and chronic lovastatin treatment attenuated the phoshorylation of Akt; however, acute but not chronic lovastatin treatment increased the phosphorylation of p42 MAPK/ERK. We conclude that, although lovastatin may lead to cardioprotection, it interferes with the mechanisms of cardiac adaptation to ischemic stress. Copyright © 2008 the American Physiological Society.
Authors & Co-Authors
Kocsis, Gabriella F.
Hungary, Szeged
Cardiovascular Research Group, Szeged
Pipis, Judit
Hungary, Szeged
Cardiovascular Research Group, Szeged
Fekete, Veronika
Hungary, Szeged
Cardiovascular Research Group, Szeged
Kovács-Simon, Andrea
Hungary, Szeged
Cardiovascular Research Group, Szeged
Odendaal, Louise
South Africa, Bellville
Cape Peninsula University of Technology
Molnár, Éva
Hungary, Szeged
Szegedi Tudományegyetem Szte
Giricz, Zoltán
Hungary, Szeged
Cardiovascular Research Group, Szeged
Janáky, Tamás
Hungary, Szeged
Szegedi Tudományegyetem Szte
van Rooyen, Jacques
South Africa, Bellville
Cape Peninsula University of Technology
Csont, Tamás
Hungary, Szeged
Cardiovascular Research Group, Szeged
Ferdinandy, Peter
Hungary, Szeged
Cardiovascular Research Group, Szeged
Statistics
Citations: 69
Authors: 11
Affiliations: 3
Identifiers
Doi:
10.1152/ajpheart.00862.2007
ISSN:
03636135
e-ISSN:
15221539
Research Areas
Noncommunicable Diseases