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  • 1990-1994  (2)
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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 17 (1990), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. In order to assess whether the observed hypotensive response in some patients given human granulocyte-macrophage colony stimulating factor (GM-CSF) is caused by a direct vascular effect of the GM-CSF, the effects of mouse and human GM-CSF were examined in rat aortic rings and human saphenous veins respectively.2. No effects of GM-CSF were observed, either in the presence or absence of endothelium, on responses to the α-adrenoceptor agonist phenylephrine.3. These data suggest that GM-CSF does not have direct effects on either vascular endothelium or smooth muscle, and that a direct vascular effect of GM-CSF is not the explanation for the observed clinical response.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 20 (1993), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. The aim of these experiments was to determine if the vasorelaxation of the rat isolated aorta induced by sufentanil or alfentanil is mediated by the endothelium, and, if not, by α-adrenoceptor blockade, or a direct effect on the smooth muscle.2. Both sufentanil (from 10−7 mol/L to 10−4 mol/ L) and alfentanil (from 10−7 mol/ L to 3 × 10−4 mol/L) relaxed rings, where endothelium was intact and precontracted with 40 mmol/L KC1, in a concentration-related manner. Similarly, sufentanil and alfentanil relaxed rings, in the presence or absence of endothelium, which had been precontracted with phenylephrine.3. Naloxone (10−4 mol/L) had no significant effect on the relaxation induced by either sufentanil or alfentanil.4. In a similar manner as phentolamine, pretreatment with sufentanil protected α-adrenoceptors from blockade by phenoxybenzamine (PBZ) in both endothelium intact and denuded rings, but the estimated potency of sufentanil was approximately 100-fold less than that of phentolamine in α-adrenoceptor protection. Treatment with alfentanil did not produce any receptor protection.5. We concluded that, in the rat aorta, vascular relaxation induced by sufentanil is mediated by both α-adrenoceptor blockade and a direct effect on smooth muscle, whilst the relaxant effect of alfentanil is caused by direct effects alone. We also concluded that the endothelium has little role in relaxation produced by either drug.
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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