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硫利达嗪引起的射精功能障碍是外周源性的吗?

Is thioridazine-induced ejaculation failure peripheral in origin?

作者信息

Nakanishi H, Kaneko M

出版信息

Res Commun Chem Pathol Pharmacol. 1978 Mar;19(3):549-52.

PMID:653110
Abstract

The contractile response of rabbit vas deferens to the field stimulation was almost equally depressed by thioridazine and chlorpromazine. Phenoxybenzamine in a dose of 10(-7) g/ml augmented the response slightly, while in a dose of 10(-6) g/ml slightly depressed. The contractile response to exogenously administered noradrenaline was remarkably depressed by thioridazine and chlorpromazine and completely abolished by phenoxybenzamine. Almost equal potencies of sympatholytic effects of thioridazine and chlorpromazine may exclude the possibility that thioridazine-induced ejaculation failure, which is higher incidence than the failure induced by chlorpromazine, is due to its inhibitory action on peripheral adrenergic mechanism.

摘要

硫利达嗪和氯丙嗪对兔输精管的场刺激收缩反应的抑制作用几乎相同。剂量为10(-7)克/毫升的酚苄明可使反应稍有增强,而剂量为10(-6)克/毫升时则稍有抑制。硫利达嗪和氯丙嗪可显著抑制对外源性给予去甲肾上腺素的收缩反应,酚苄明则可使其完全消失。硫利达嗪和氯丙嗪的抗交感作用效力几乎相同,这可能排除了硫利达嗪引起射精失败(其发生率高于氯丙嗪引起的失败)是由于其对外周肾上腺素能机制的抑制作用这一可能性。

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