Direct vascular and cardioprotective effects of rosuvastatin, a new HMG-CoA reductase inhibitor

摘要: Abstract 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 inhibitors promote vascular function through enhanced NO production. However, it is unclear whether all statins share this beneficial side effect or limited to “natural” statins. Methods Wild-type mice (n = 158) were subjected 30 min regional ischemia 24 h reperfusion. Mice treated with various doses rosuvastatin (0.1, 0.5, 1.0, 2.0, 5.0 mg/kg) 18 before Results Rosuvastatin significantly increased from endothelium following acute administration mice. In addition, synthase (eNOS) messenger ribonucleic acid levels. Myocardial necrosis was reduced by approximately 40% therapy. attenuated injury when administered 6 h, but not 0 3 ischemia. additional studies, did affect infarct size in eNOS-deficient compared vehicle-treated eNOS Conclusions These data demonstrate increases attenuates reperfusion