BACKGROUND: Although successful restoration of blood flow is mandatory for salvage of ischemic tissues, reperfusion can paradoxically place tissues at risk of further injury. Brief periods of ischemia applied at the onset of reperfusion have been shown to reduce ischemia-reperfusion (IR) injury, a phenomenon called postconditioning. Statin showed that reduces infarction size and increase myocardial tissue perfusion. The aim of this study is to determine whether postconditioning or statin protects against endothelial IR injury in human. METHODS: Brachial artery endothelial function was assessed by high-resolution ultrasound to measure flow-mediated dilation (FMD) in response to forearm reactive hyperemia. FMD was measured before and after IR (20 minutes of arm ischemia followed by 20 minutes of reperfusion) in 18 healthy volunteers (mean 26짹4 years, all male). To test the protective effects of postconditioning, 3 cycles of reperfusion followed by ischemia (each lasting 10 seconds) were applied immediately after 20 minutes of arm ischemia. And, To test the protective effects of statin, rosuvastatin 20mg daily were allowed for 2 weeks. RESULTS: Routine laboratory exam has not shown abnormal finding after treatment. Total cholesterol (184짹69 vs 121짹28 mg/dL, p<0.01) and LDL-cholesterol (108짹24 vs 66짹25 mg/dL, p<0.01) were significantly decreased. IR caused endothelial dysfunction (FMD: 9.29짹2.6% in pre-IR, 5.70짹3.1% in post-IR, P<0.049; n=18), which was prevented by postconditioning applied as 10-second cycles of reperfusion/ischemia (FMD: 8.72짹2.9% in pre-IR, 6.73짹2.4% in post-IR, p=0.06, n=18). But, No Protection was observed when the application of IR injury after 2 weeks rosuvastatin treatment (FMD: 10.71짹3.1% in pre-IR, 6.28짹1.8% in post-IR, P<0.01; n=18) CONCLUSION: This study demonstrates that postconditioning can protect against endothelial IR injury in humans. but short-term rosuvastatin treatment can't.