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adrenaline/nekroza
Veza se sprema u međuspremnik
Page 1 od 141 rezultati
Beta-adrenergic receptors mediate in vivo the adrenaline inhibition of lipopolysaccharide-induced tumor necrosis factor release.
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Adrenaline has been shown to inhibit the release of tumor necrosis factor (TNF) elicited by lipopolysaccharide (LPS) when tested in vitro on cultured human blood cells and rat macrophages. In this report we have examined the effect of the in vivo administration of adrenaline on TNF serum levels
Adrenaline suppression of the macrophage nitric oxide response to lipopolysaccharide is associated with differential regulation of tumour necrosis factor-alpha and interleukin-10.
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Adrenaline is a catecholamine hormone secreted by the adrenal medulla in response to acute stress. Previous studies have shown that adrenaline suppresses the nitric oxide (NO) response of murine macrophages (M phi s) stimulated in vitro with lipopolysaccharide (LPS). We have now extended these
[Necrosis in fingers and toes following local anaesthesia with adrenaline--an urban legend?].
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BACKGROUND
It is often maintained that a local anaesthetic (usually lidocaine) with adrenaline must not be used in fingers and toes because it may cause necrosis due to vascular spasm in end arteries. This review article is an attempt to find evidence to support this warning.
METHODS
Relevant
The effect of a potent inhibitor of platelet aggregation, BL-3459, on adrenaline-induced myocardial necrosis in beagle dogs.
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The effect of a potent inhibitor of platelet aggregation, BL-3459, on adrenaline-induced myocardial necrosis was investigated in beagle dogs. BL-3459, an alpha-adrenergic receptor blocking agent, phenoxybenzamine, and a beta-adrenergic receptor blocking agent, propranolol, were compared for their
Protective effect of inosine on adrenaline-induced myocardial necrosis.
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The influence of inosine (200 and 400 mg/kg i.p.) on adrenaline-induced myocardial necrosis in rats was studied. Adrenaline in a single dose (1 and 2 mg/kg s.c.) produced heart cell necrosis estimated by plasma activities of CPK-MB, CPK, blood lactates concentration and histopathological
Regulation of tumor necrosis factor production by adrenaline and beta-adrenergic agonists.
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The effects of adrenaline and isoproterenol, a specific beta-adrenergic agonist, on TNF production were investigated. Both agents inhibited the production of TNF by human blood and THP-1 cells stimulated by LPS. The effect of adrenaline was prevented by a beta-receptor antagonist, but not by an
[Local anesthetics with added adrenaline during halothane anesthesia. Assessment of the risk of necrosis and systemic side effects when these preparations are employed peripherally].
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Adrenaline necrosis.
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[Study of catecholamines in the organs of the rat in adrenaline-induced necrosis of the myocardium].
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Porokeratosis (Mibelli), adrenaline necrosis, atopic eczema.
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Skin necrosis in nor-adrenaline therapy.
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EPIDERMAL NECROSIS DUE TO NOR-ADRENALINE.
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[Immunomorphological and histoenzymological study of adrenaline-induced myocardial necrosis].
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[On the immumology of repeated adrenaline necrosis of the myocardium].
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[Immunomorphological and histoenzymological analysis of adrenaline-induced myocardial necrosis (experimental study)].
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