Simvastatin preserves the ischemic-reperfused myocardium in normocholesterolemic rat hearts.

@article{Lefer1999SimvastatinPT,
  title={Simvastatin preserves the ischemic-reperfused myocardium in normocholesterolemic rat hearts.},
  author={A. Lefer and B. Campbell and Y. Shin and R. Scalia and R. Hayward and D. Lefer},
  journal={Circulation},
  year={1999},
  volume={100 2},
  pages={
          178-84
        }
}
BACKGROUND Ischemia followed by reperfusion in the presence of polymorphonuclear leukocytes (PMNs) results in cardiac contractile dysfunction as well as cardiomyocyte injury. These deleterious effects are due in large part to endothelial dysfunction leading to the upregulation of cell adhesion molecules and subsequent neutrophil-endothelium interaction. At clinically relevant doses, simvastatin, an HMG-CoA reductase inhibitor, has been shown to lower serum cholesterol levels and normalize… Expand
Effects of simvastatin on cardiohemodynamic responses to ischemia–reperfusion in isolated rat hearts
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TLDR
Pre-ischemic treatment with simvastatin reduces MI size via NO production and could be a useful drug for coronary artery disease patients without dyslipidemia as it has direct protective effects. Expand
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TLDR
Data show that simvastatin and manidipine interact positively in protecting the rat heart from ischemia-reperfusion injury, possibly through increased prostaglandin and nitric oxide formation by the vascular endothelial cells. Expand
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TLDR
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TLDR
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TLDR
Evidence is provided that rosuvastatin significantly attenuates PMN-induced cardiac contractile dysfunction in the isolated perfused rat heart and Nω-nitro-l-arginine methyl ester blocked these cardioprotective effects. Expand
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TLDR
The potential to pretreat recipients of lung transplantation with statins to ameliorate reperfusion injury is promising and the protective effects of simvastatin are likely mediated by modulation of endothelial nitric oxide synthase. Expand
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TLDR
The results of the present study reveal that simvastatin may ameliorate myocardial I/R injury in rats via interfering with  inflammatory responses  which induced by I-R injury. Expand
The Anti-Anginal Drug Trimetazidine Reduces Neutrophil-Mediated Cardiac Reperfusion Injury
TLDR
Cardiac oxygen radical production at reflow (by electron paramagnetic resonance spectroscopy) was also reduced by trimetazidine, independently of direct scavenger effects, indicating that trimetrazidine can protect postischemic hearts from neutrophil-mediated injury. Expand
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PMN-mediated myocardial contractile dysfunction is attenuated by NO and exacerbated by blockade of NO synthesis, as evidence by a 93% reduction in LVDP at 45 minutes of reperfusion and a 91% reduce in PRP. Expand
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  • Chemistry, Medicine
  • FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 1991
TLDR
Endothelial dysfunction occurs after myocardial ischemia and reperfusion characterized by a marked reduction in endothelium‐dependent relaxation (EDR), which is then amplified by neutrophil adherence and diapedesis into the isChemic region enhancing post‐reperfusion ischemic injury. Expand
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TLDR
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