noradrenaline/necrosis

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

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

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 (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

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

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

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

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

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

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