Abstract
Purpose: Cardioprotective effects of HMG-CoA reductase inhibitors on myocardial ischemia-reperfusion (MI-R) injury might result from increased release of NO via the eNOS bioavailability. In this study, we investigated whether fluvastatin could attenuate MI-R injury through the NO pathway, and whether increased NOS bioavailability might be related to its ability to stabilize eNOS mRNA or to activate the phosphatidylinositide (PI) 3-kinase/Akt pathway.
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