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menadione/infarction
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Menadione mimics the infarct-limiting effect of preconditioning in isolated rat hearts.
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The role of mitochondrial free radicals in the cardioprotective effect of ischemic preconditioning was examined in isolated buffer-perfused rat hearts. Infarct size in control rat hearts subjected to 30 min of regional ischemia and 120 min of reperfusion was 32.6 +/- 3.4% of the risk zone. Ischemic
Extracorporeal Shock Wave-Supported Adipose-Derived Fresh Stromal Vascular Fraction Preserved Left Ventricular (LV) Function and Inhibited LV Remodeling in Acute Myocardial Infarction in Rat.
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This study tested the hypothesis that extracorporeal shock wave- (ECSW-) assisted adipose-derived stromal vascular fraction (SVF) therapy could preserve left ventricular ejection fraction (LVEF) and inhibit LV remodeling in a rat after acute myocardial infarction (AMI). Adult male SD rats were
The relative order of mK(ATP) channels, free radicals and p38 MAPK in preconditioning's protective pathway in rat heart.
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OBJECTIVE
Ischemic preconditioning (PC) reduces myocardial infarction by a mechanism that involves opening of mitochondrial ATP-dependent potassium channels (mK(ATP)), reactive oxygen species (ROS), and possibly activation of p38 mitogen-activated protein kinase (p38 MAPK). The actual order of these
[Effect of free radicals on the permeability of the blood brain barrier--using in vitro blood brain barrier model of human-SOD transgenic mouse].
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Free radicals have been implicated in pathogenesis of vasogenic edema caused by post-ischemic reperfusion injury. It has been reported that Cu-Zn superoxide dismutase transgenic mouse (tg-mouse) which is overexpressing Cu-Zn SOD, prevents post ischemic brain edema and decreases infarct size in
Impairment of diazoxide-induced formation of reactive oxygen species and loss of cardioprotection in connexin 43 deficient mice.
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Protection by ischemic preconditioning is lost in cardiomyocytes and hearts of heterozygous connexin 43 deficient (Cx43+/-) mice. Because connexin 43 (Cx43) is localized in cardiomyocyte mitochondria and mitochondrial Cx43 content is increased with ischemic preconditioning, we now tried to identify
Free radical-mediated neurotoxicity may be caused by inhibition of mitochondrial dehydrogenases in vitro and in vivo.
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We previously demonstrated that copper facilitated the formation of reactive oxygen species, and inhibited pyruvate dehydrogenase and alpha-ketoglutarate dehydrogenase in vitro and in animal models of Wilson's disease in vivo. However, direct Cu(2+) toxicity has only been demonstrated for Wilson's
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