慢性乙醇处理可改变大鼠脑微血管中β受体的数量。

Substance and alcohol actions/misuse Pub Date : 1984-01-01
L Lucchi, A Cazzaniga, G B Picotti, V Covelli, M S Magnoni, L Borriero, P F Spano, M Trabucchi
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引用次数: 0

摘要

研究了慢性乙醇消耗对大鼠脑微血管(125I)-碘羟基苄基品多洛尔与β -肾上腺素能受体结合的影响。结果表明,慢性乙醇处理增加了脑微血管中β受体的数量,但不改变β -肾上腺素能受体配体结合位点的结合亲和力。这种影响显然与外周肾上腺素能张力的变化无关,因为在乙醇处理的动物和对照动物之间,血小板肾上腺素或去甲肾上腺素浓度没有差异。脑微血管β受体密度的增加可能导致慢性乙醇中毒期间脑血流量和耗氧量的改变。
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Chronic ethanol treatment changes the number of beta-receptors in rat brain microvessels.

The effect of chronic ethanol consumption on the binding (125I)-iodohydroxybenzylpindolol to beta-adrenergic receptors in rat brain microvessels has been studied. The results show that chronic ethanol treatment increases the number of beta-receptors present in brain microvessels without changing the binding affinity of the binding site for the beta-adrenoceptor ligand. This effect is apparently not associated with changes in peripheral adrenergic tone, since no differences in platelet epinephrine or norepinephrine concentrations were found between ethanol-treated and control animals. An increase in beta-receptor density in brain microvessels might contribute to the alterations of cerebral blood flow and oxygen consumption reported during chronic ethanol intoxication.

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Occurrence of trace indoles in mammals. Effects of L-tyrosine on brain monoamines in rats given intravenous amphetamine. Chronic maternal ethanol administration in the rat decreases the stimulation by (-) epinephrine of glycogen phosphorylase a in the livers of the progeny during development. Enkephalinergic-dopaminergic "reward" pathways: a critical substrate for the stimulatory, euphoric and memory-enhancing actions of alcohol--a hypothesis. Chronic ethanol treatment changes the number of beta-receptors in rat brain microvessels.
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