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noradrenaline/necrosis
L'enllaç es desa al porta-retalls
Pàgina 1 des de 237 resultats
Interleukin-1 beta and tumor necrosis factor-alpha inhibit the release of [3H]-noradrenaline from mice isolated atria.
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In the present study, we have investigated the ability of four cytokines, interleukin-1 beta, interleukin-2, interleukin-6 and tumor necrosis factor-alpha, to modulate the stimulation-induced outflow of radioactivity from isolated superfused mouse atria which where pre-incubated with
Interleukin-1 beta and tumor necrosis factor-alpha inhibit the release of [3H]-noradrenaline from isolated human atrial appendages.
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In the present study, we have investigated the ability of human recombinant interleukin-1 beta (hIL-1 beta) and human recombinant tumor necrosis factor-alpha (hTNF-alpha) to modulate the stimulation-induced (S-I) outflow of [3H]-noradrenaline ([3H]-NA) from isolated superfused human atria. Pieces of
Effect of noradrenaline and isoproterenol on lipopolysaccharide-induced tumor necrosis factor-alpha production in whole blood from patients with chronic heart failure and the role of beta-adrenergic receptors.
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Increased levels of tumor necrosis factor-alpha (TNF-alpha) correlate with poor prognoses in chronic heart failure (CHF). This study demonstrated that noradrenaline and isoproterenol inhibit TNF-alpha production in patients with CHF in ex vivo whole blood in a dose-dependent fashion. The
Noradrenaline metabolism in neocortex and hippocampus following transient forebrain ischemia in rats: relation to development of selective neuronal necrosis.
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Noradrenaline (NA) metabolism in the neocortex and hippocampus was examined in rats at 1, 24, and 48 h following 15 min of reversible forebrain ischemia. As assessed by the ratio of accumulated 3,4-dihydroxyphenylalanine (DOPA) to the tissue NA level after inhibition of DOPA decarboxylase, the NA
Role of noradrenaline in the pathogenesis of skin flap ischemic necrosis in the pig.
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Clinically, ischemic necrosis is one of the most common complications in skin flap surgery, but the etiology is still unclear. The objective of the present experiments was to study the important role of the locally released noradrenaline in the pathogenesis of ischemic necrosis in acute and delayed
Regulation of adenylyl cyclase by noradrenaline and tumour necrosis factor alpha in rat cardiomyocytes.
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The regulation of adenylyl cyclase components and of adenylyl cyclase activity by noradrenaline and tumour necrosis factor alpha (TNF alpha) was studied in rat cardiomyocytes. Long-term treatment of rat cardiomyocytes in the presence of noradrenaline leads, in addition to a down-regulation of beta
Protective effects of noradrenaline against tumor necrosis factor-alpha-induced apoptosis in cultured rat brown adipocytes: role of nitric oxide-induced heat shock protein 70 expression.
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OBJECTIVE
To elucidate the effects and molecular mechanism(s) by means of which noradrenaline (NA) protects against the tumor necrosis factor (TNF)-alpha-induced apoptosis of brown adipocytes.
METHODS
Brown fat precursor cells were isolated from young rats; 2.5 million cells were added to each
[Microvascular injury in hyperthermia by injecting warm water using noradrenaline into tumor feeding artery-induced tumor necrosis of Walker-256].
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Wistar rats were injected sc, with cells from Walker-256, which is resistant to hyperthermia. When hyperthermia was achieved by immersing the tumor at 44 degrees C for 60 minutes after injecting MMC (0.5 mg/kg), tumor growth was markedly suppressed in D-8 group, which formed many tumor vessels, but
Noradrenaline inhibits lipopolysaccharide-induced tumor necrosis factor and interleukin 6 production in human whole blood.
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Sepsis and lipopolysaccharide (LPS) trigger the systemic release of both cytokines and catecholamines. Cytokines are known to be capable of eliciting a stress hormone response in vivo. The present study sought insight into the effect of noradrenaline on LPS-induced release of tumor necrosis factor
Protective effects of slow channel calcium antagonists on noradrenaline induced myocardial necrosis.
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Catecholamine excess results in two distinct forms of coagulative myocytolysis, apparently due to increased membrane permeability followed by a large influx of calcium. To determine if three slow channel calcium antagonists, verapamil, nifedipine, and diltiazem, could reduce the calcium overload and
[REGIONAL NECROSIS FOLLOWING NORADRENALINE ADMINISTRATION].
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Treatment of noradrenaline infusion necrosis.
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[Cutaneous necrosis caused by noradrenaline infusion].
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Fibrinoid necrosis of the vascular wall induced by noradrenaline.
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Soft tissue necrosis with noradrenaline and its prevention with isoxsuprine.
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