| 박정수, 김원, 박현희, 조은경, 정은미, 박상현, 정안덕, 조상철, 황선호, 김완 |
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. The effect of statin is that it improves endothelial function and reduce proinflammatroy cytokines. The aim of this study is to determine whether short-term statin protects against endothelial IR injury in humans, in vivo.
Methods: Brachial artery endothelial function was assessed by high-resolution ultrasound to measure flow-mediated dilation(FMD) in response to forearm reactive hyperemia. At first, for the IR injury examination, FMD was measured before and after IR (20 minutes of arm ischemia followed by 20 minutes of reperfusion) in 24 healthy volunteers (mean 26±4 years, all male). To test the protective effects of ischemic preconditioning of statin, rosuvastatin 20 mg daily were applied for 2 weeks. And then, for the effect of ischemic pre-conditioning of rosuvastatin, 2nd FMD was examinated before and after IR.
Results: Routine laboratory exam has not shown a significant change in clinical finding after rosuvastatin treatment. However, total cholesterol (184.6±69.1 vs. 121.6±28.8 mg/dL, p<0.01), LDL cholesterol (108±24 vs. 66±25 mg/dL, p<0.01) and triglyceride (113.3±66.9 vs. 89.74±3.9 mg/dL, p<0.01) were significantly decreased after rosuvastatin treatment. Baseline FMD before pre-IR was improved by rosuvastatin treatment of 2 weeks (from 9.29±2.6% to 10.71±3.1%, p<0.05). The endothelial dysfunction (FMD) was observed by IR injury (9.29±2.6% in pre-IR, 5.70±3.1% in post-IR, p<0.05; n=24). No protective effect was observed when the application of IR after rosuvastatin treatment (FMD: 10.71±3.1% in pre-IR, 6.28±1.8% in post-IR, P<0.01; n=24).
Conclusions: This study demonstrates that short-term statin treatment imrpoved endothelial dysfunction, but can’t protect against endothelial IR injury in humans.
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