ArticleBritish journal of pharmacology2006
Pretreatment with simvastatin reduces myocardial no-reflow by opening mitochondrial K(ATP) channel.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 47 citations in OpenAlex.
- Article
- New and revisited approaches to preserving the reperfused myocardium.Nature reviews. Cardiology · 2017Review
- Simvastatin Ameliorates Diabetic Cardiomyopathy by Attenuating Oxidative Stress and Inflammation in Rats.Oxidative medicine and cellular longevity · 2017Article
- Cardiac microvascular barrier function mediates the protection of Tongxinluo against myocardial ischemia/reperfusion injury.PloS one · 2015Article
- ATP-dependent potassium channels are implicated in simvastatin pretreatment-induced inhibition of apoptotic cell death after renal ischemia/reperfusion injury.Medical journal of the Islamic Republic of Iran · 2015Article
- Simvastatin prevents isoproterenol-induced cardiac hypertrophy through modulation of the JAK/STAT pathway.Drug design, development and therapy · 2015Article
- Effects of single-dose atorvastatin on interleukin-6, interferon gamma, and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2014Article
- Consequences of Ischemic Preconditioning of Kidney: Comparing between Male and Female Rats.Iranian journal of basic medical sciences · 2012Article
- Phosphorylation of endothelial NOS contributes to simvastatin protection against myocardial no-reflow and infarction in reperfused swine hearts: partially via the PKA signaling pathway.Acta pharmacologica Sinica · 2012Article
- Thiazolidinedione drugs promote onset, alter characteristics, and increase mortality of ischemic ventricular fibrillation in pigs.Cardiovascular drugs and therapy · 2012Article
- Role of endogenous vitamin E in renal ischemic preconditioning process: differences between male and female rats.Iranian biomedical journal · 2012Article
- Effect of statin therapy on reperfusion arrhythmia in patients who underwent successful primary angioplasty.Clinical research in cardiology : official journal of the German Cardiac Society · 2008Article
- Statin therapy and myocardial no-reflow.British journal of pharmacology · 2006Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeSimvastatin, 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
resultsCompared 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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