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Strana 1 od 42 výsledky
[Elimination of disorders of the elasticity and contractile function of nonischemic portions of the heart in myocardial infarct by using glucose and uridine].
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A study of an isolated auricle showed that one day after the infarction the extensibility of the atrial myocardium was reduced, the Starling curve was depressed to result in about a two-fold decrease of the peak systolic tension, and atrial myocardial resistance to hypoxia and excessive calcium was
Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.
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We have previously found that uridine 5'-triphosphate (UTP) significantly reduced cardiomyocyte death induced by hypoxia via activating P2Y(2) receptors. To explore the effect of UTP following myocardial infarction (MI) in vivo we studied four groups: sham with or without LAD ligation, injected with
Blunted coronary vasodilator response to uridine adenosine tetraphosphate in post-infarct remodeled myocardium is due to reduced P1 receptor activation.
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We previously demonstrated that uridine adenosine tetraphosphate (Up4A) exerts a potent vasodilator effect in the healthy porcine coronary vasculature. Since the coronary microvascular effects of Up4A after myocardial infarction (MI) are unknown, the present study investigated the response to Up4A
Positive inotropic effects by uridine triphosphate (UTP) and uridine diphosphate (UDP) via P2Y2 and P2Y6 receptors on cardiomyocytes and release of UTP in man during myocardial infarction.
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The aim of this study was to examine a possible role for extracellular pyrimidines as inotropic factors for the heart. First, nucleotide plasma levels were measured to evaluate whether UTP is released in patients with coronary heart disease. Then, inotropic effects of pyrimidines were examined in
Uridine: a marker of myocardial viability after coronary occlusion and reperfusion.
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Tissue accumulation of radiolabeled uridine, a precursor of uracil, reflects ribonucleic acid (RNA) synthesis and may be a marker of viability. To test this hypothesis, myocardial accumulation of H-3 uridine was compared to deoxyglucose uptake and histopathology in an experimental model of
Nogo-A is associated with secondary degeneration of substantia nigra in hypertensive rats with focal cortical infarction.
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We investigated the association of Nogo-A protein, a myelin-associated inhibitor of axon regeneration, with secondary damage of the ipsilateral substantia nigra pars reticulata (SNr) after distal middle cerebral artery occlusion (dMCAO) in adult stroke-prone, renovascular hypertensive rats.
Improved left ventricular function after transplantation of microspheres and fibroblasts in a rat model of myocardial infarction.
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As a novel and promising therapeutic strategy for heart failure, the application of different cell types is the subject of increasing research interest. In this study we investigated the effect of several cell types and microspheres (uniform polystyrene microspheres, 10 microm diameter) transplanted
17-beta-estradiol increases cardiac remodeling and mortality in mice with myocardial infarction.
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OBJECTIVE
This study was designed to examine the effects of estrogen replacement on infarct size, ventricular remodeling, and mortality after myocardial infarction (MI) in mice.
BACKGROUND
Observational and clinical studies suggest that the cardiovascular effects of hormone replacement therapy can
UTP reduces infarct size and improves mice heart function after myocardial infarct via P2Y2 receptor.
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Pyrimidine nucleotides are signaling molecules, which activate G protein-coupled membrane receptors of the P2Y family. P2Y(2) and P2Y(4) receptors are part of the P2Y family, which is composed of 8 subtypes that have been cloned and functionally defined. We have previously found that
Uridine protects cortical neurons from glucose deprivation-induced death: possible role of uridine phosphorylase.
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We previously reported that uridine blocked glucose deprivation-induced death of immunostimulated astrocytes by preserving ATP levels. Uridine phosphorylase (UPase), an enzyme catalyzing the reversible phosphorylation of uridine, was involved in this effect. Here, we tried to expand our previous
Uridine 5'-triphosphate (UTP) protects against cerebral ischemia reperfusion injury in rats.
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OBJECTIVE
To test the hypothesis that uridine 5'-triphosphate (UTP) had a protective effect on cerebral ischemia reperfusion (IR) injury in rats.
METHODS
Ischemia was induced by intraluminal suture of middle cerebral artery occlusion (MCAO). UTP solution was delivered through an indwelling tail
Uridine-5'-triphosphate (UTP) maintains cardiac mitochondrial function following chemical and hypoxic stress.
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Previously we found that uridine-5'-triphosphate (UTP) significantly decreased cultured cardiomyocyte death, induced by hypoxia via activating P2Y(2) receptors, reduced infarct size and maintained higher ATP levels in an in vivo model. Mitochondrial contribution to the progression of cardiomyocyte
Adenosine diphosphate reduces infarct size and improves porcine heart function after myocardial infarct.
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Acute myocardial infarction continues to be a major cause of morbidity and mortality. Timely reperfusion can substantially improve outcomes and the administration of cardioprotective substances during reperfusion is therefore highly attractive. Adenosine diphosphate (ADP) and uridine-5-triphoshate
Divergent coronary flow responses to uridine adenosine tetraphosphate in atherosclerotic ApoE knockout mice.
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Uridine adenosine tetraphosphate (Up4A) exerts potent relaxation in porcine coronary arteries that is reduced following myocardial infarction, suggesting a crucial role for Up4A in the regulation of coronary flow (CF) in cardiovascular disorders. We evaluated the vasoactive effects of Up4A on CF in
Altered purinergic signaling in uridine adenosine tetraphosphate-induced coronary relaxation in swine with metabolic derangement.
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We previously demonstrated that uridine adenosine tetraphosphate (Up4A) induces potent and partially endothelium-dependent relaxation in the healthy porcine coronary microvasculature. We subsequently showed that Up4A-induced porcine coronary relaxation was impaired via downregulation of P1 receptors
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