Inhibition of Tumor Necrosis Factor-α Improves Postischemic Recovery of Hypertrophied Hearts
نویسندگان
چکیده
منابع مشابه
Inhibition of Tumor Necrosis Factor-a Improves Postischemic Recovery of Hypertrophied Hearts
Background—Tumor necrosis factor (TNF)-a has been implicated in the pathogenesis of heart failure and ischemiareperfusion injury. Effects of TNF-a are initiated by membrane receptors coupled to sphingomyelinase signaling and include altered metabolism and calcium cycling, contractile dysfunction, and cell death. We postulate that pressureoverload hypertrophy results in increased myocardial TNF-...
متن کاملInhibition of tumor necrosis factor-alpha improves postischemic recovery of hypertrophied hearts.
BACKGROUND Tumor necrosis factor (TNF)-alpha has been implicated in the pathogenesis of heart failure and ischemia-reperfusion injury. Effects of TNF-alpha are initiated by membrane receptors coupled to sphingomyelinase signaling and include altered metabolism and calcium cycling, contractile dysfunction, and cell death. We postulate that pressure-overload hypertrophy results in increased myoca...
متن کاملDichloroacetate improves postischemic function of hypertrophied rat hearts.
OBJECTIVES We sought to determine whether improving coupling between glucose oxidation and glycolysis by stimulating glucose oxidation during reperfusion enhances postischemic recovery of hypertrophied hearts. BACKGROUND Low rates of glucose oxidation and high glycolytic rates are associated with greater postischemic dysfunction of hypertrophied as compared with nonhypertrophied hearts. MET...
متن کاملTrimetazidine normalizes postischemic function of hypertrophied rat hearts.
The fraction of glucose passing through glycolysis that is oxidized is low in hypertrophied hearts, a pattern of glucose use associated with poor postischemic contractile function. We tested the hypothesis that trimetazidine, a partial 3-ketoacyl coenzyme A thiolase inhibitor, would stimulate glucose oxidation and, thereby, improve fractional glucose oxidation and postischemic function of hyper...
متن کاملInhibition of PLC improves postischemic recovery in isolated rat heart.
The Ca2+-dependent PLC converts phosphatidylinositol 4,5-bisphosphate to diacylglycerol (DAG) and inositol 1,4,5-trisphosphate [Ins(1,4,5)P3]. Because these products modulate Ca2+ movements in the myocardium, PLC may also contribute to a self-perpetuating cycle that exacerbates cardiomyocyte Ca2+-overload and subsequent cardiac dysfunction in ischemia-reperfusion (I/R). Although we have reporte...
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ژورنال
عنوان ژورنال: Circulation
سال: 2001
ISSN: 0009-7322,1524-4539
DOI: 10.1161/hc37t1.094851