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Figure 5 The role of endothelial nitric oxide synthase (eNOS) in the attenuation of myocardial ischemia–reperfusion injury following injection with rosuvastatin. Mice deficient in eNOS were administered either saline vehicle (n = 5) or 0.5 mg/kg rosuvastatin (n = 5) 18 h before being subjected to myocardial ischemia and reperfusion. Rosuvastatin failed to significantly (p = NS) alter the extent of myocardial injury in eNOS-deficient mice. AAR = areas-at-risk; LV = left ventricle; NEC = necrosis.
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