Literature DB >> 16921391

Pretreatment with simvastatin reduces myocardial no-reflow by opening mitochondrial K(ATP) channel.

J-L Zhao1, Y-J Yang, C-J Cui, S-J You, R-L Gao.   

Abstract

BACKGROUND AND
PURPOSE: Simvastatin, a cholesterol-lowering agent, can protect against endothelial dysfunction. However, the effects of simvastatin treatment on the restoration of blood flow to ischemic myocardium are not known. This study sought to assess such effects of simvastatin on an experimental model of myocardial no-reflow and to explore possible mechanisms. EXPERIMENTAL APPROACH: Coronary ligation area and area of no-reflow were determined by myocardial contrast echocardiography in vivo and by histology in mini-pigs randomized into 7 study groups: controls, pretreated with simvastatin for 2 days, treated with 5-hydroxydecanoate (5-HD, the selective mitochondrial K(ATP) channel blocker), treated with simvastatin+5-HD, treated with HMR 1883 (the selective sarcolemmal K(ATP) channel blocker), treated with simvastatin+HMR 1883 and a sham-operated group. The myocardial no-reflow model was induced with 3 h occlusion of the left anterior descending coronary artery followed by 2 h reperfusion. KEY
RESULTS: Compared with the control group, simvastatin significantly increased coronary blood flow, decreased the area of no-reflow assessed echocardiographically and reduced the necrotic area, by histology. There was no significant difference in these outcomes between simvastatin and simvastatin+HMR 1883 groups. In contrast, 5-HD abolished the effect of simvastatin. CONCLUSIONS AND IMPLICATIONS: Simvastatin can reduce the area and myocardial no-reflow after ischaemia and reperfusion. This beneficial effect is due to its activation of mitochondrial K(ATP) channels.

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Year:  2006        PMID: 16921391      PMCID: PMC2014278          DOI: 10.1038/sj.bjp.0706862

Source DB:  PubMed          Journal:  Br J Pharmacol        ISSN: 0007-1188            Impact factor:   8.739


  33 in total

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