Journal
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
Volume 40, Issue 6, Pages 1172-1178Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/S0735-1097(02)02115-0
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Funding
- NHLBI NIH HHS [R01 HL 60849] Funding Source: Medline
- NIDDK NIH HHS [P01 DK43785] Funding Source: Medline
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OBJECTIVES We examined the possible effects of a novel 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitor, rosuvastatin, on endothelial nitric oxide (NO) production and myocardial ischemia-reperfusion injury. BACKGROUND Recent studies suggest that HMG-CoA reductase inhibitors promote vascular endothelial function through enhanced endothelial NO production. However, it is unclear whether all statins share this beneficial side effect or whether this effect is limited to the natural statins. METHODS Wild-type mice (n = 158) were subjected to 30 min of regional myocardial ischemia and 24 h of reperfusion. Mice were treated with various doses of rosuvastatin (0.1, 0.5, 1.0, 2.0, and 5.0 mg/kg) 18 h before myocardial ischemia and reperfusion. RESULTS Rosuvastatin significantly increased NO production from the vascular endothelium. following acute administration to mice. In addition, rosuvastatin increased myocardial endothelial nitric oxide synthase (eNOS) messenger ribonucleic acid levels. Myocardial necrosis was reduced by approximately 40% with rosuvastatin therapy. Rosuvastatin attenuated myocardial injury when it was administered 6 h, but not 0 h or 3 h, before myocardial ischemia. In additional studies, rosuvastatin did not affect myocardial infarct size in eNOS-deficient mice compared to vehicle-treated eNOS mice. CONCLUSIONS These data demonstrate that rosuvastatin increases vascular endothelial NO production and attenuates myocardial necrosis following ischemia and reperfusion in mice.
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