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用6-羟基多巴胺选择性破坏中枢和外周含儿茶酚胺神经元对大鼠儿茶酚胺排泄的影响

Effect of selective destruction of central and peripheral catecholamine-containing neurones with 6-hydroxydopamine on catecholamine excretion in the rat.

作者信息

Hoeldtke R, Rogawski M, Wurtman R J

出版信息

Br J Pharmacol. 1974 Feb;50(2):265-70. doi: 10.1111/j.1476-5381.1974.tb08571.x.

Abstract

1 The contribution of various tissues to some of the pools of catecholamine metabolites in urine has been estimated by measuring the excretion of these compounds by rats given DOPA-free diets and intravenous, intraventricular, or intracisternal 6-hydroxydopamine.2 Destruction of peripheral sympathetic neurones by repeated intravenous doses of 6-hydroxydopamine led to a 34% decrease in noradrenaline excretion, and a 38% decrease in 4-hydroxy-3-methoxyphenylglycol sulphate excretion. Depletion of brain noradrenaline (by 67%), after intracisternal 6-hydroxydopamine, was unassociated with changes in the excretion of noradrenaline or of 4-hydroxy-3-methoxyphenylglycol sulphate. This suggests that these compounds in rat urine are derived mainly from peripheral tissues.3 Depletion of brain dopamine (by 80%) by intraventricular 6-hydroxydopamine was associated with a 27% decrease in the excretion of homovanillic acid. Destruction of peripheral sympathetic neurones with intravenous 6-hydroxydopamine led to a 25% decrease in homovanillic acid excretion. The data suggest that the homovanillic acid in rat urine derives partially from brain dopamine and partially from dopamine released from or metabolized within sympathetic neurones.4 Neither depletion of brain dopamine, nor destruction of sympathetic neurones, caused alterations in the excretion of dopamine or dihydroxyphenylacetic acid.

摘要

1 通过测量给予无多巴饮食并经静脉、脑室内或脑池内注射6-羟基多巴胺的大鼠体内这些化合物的排泄量,估算了各种组织对尿中儿茶酚胺代谢产物某些池的贡献。

2 反复静脉注射6-羟基多巴胺破坏外周交感神经元导致去甲肾上腺素排泄量减少34%,4-羟基-3-甲氧基苯乙二醇硫酸盐排泄量减少38%。脑池内注射6-羟基多巴胺后,脑内去甲肾上腺素耗竭(减少67%)与去甲肾上腺素或4-羟基-3-甲氧基苯乙二醇硫酸盐排泄量的变化无关。这表明大鼠尿中的这些化合物主要来源于外周组织。

3 脑室内注射6-羟基多巴胺使脑内多巴胺耗竭(减少80%),与高香草酸排泄量减少27%有关。静脉注射6-羟基多巴胺破坏外周交感神经元导致高香草酸排泄量减少25%。数据表明,大鼠尿中的高香草酸部分来源于脑内多巴胺,部分来源于交感神经元释放或代谢的多巴胺。

4 脑内多巴胺耗竭或交感神经元破坏均未引起多巴胺或二羟基苯乙酸排泄量的改变。

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