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[卵巢代偿性肥大的肾上腺素能机制的药理学研究]

[Pharmacologic study of adrenergic mechanisms of compensatory hypertrophy of the ovary].

作者信息

Anisimov V N

出版信息

Biull Eksp Biol Med. 1975 Dec;80(12):44-6.

PMID:1225399
Abstract

Treatment of hemicastrated adult female rats with adrenoblockers, chlorpromazine and alpha-methyl-DOPA decreased the ovarian compensatory hypertrophy (OCH) and prevented the stilbestrol suppression of the OCH. Disulfiram (dophamine-beta-hydroxylase inhibitor) potentiated the stilbestrol suppression of the OCH. Small doses of L-DOPA stimulated the OCH, and high doses of L-DOPA and dilantin failed to act on the ACH, but potentiated the estrogeninduced OCH inhibition. It is suggested that the FSH secretion was mediated by the release of norepinephrine in the central adrenergic neurons and that the estrogen action inhibiting the FSH secretion was mediated through the stimulation of dophamine release.

摘要

用肾上腺素阻滞剂、氯丙嗪和α-甲基多巴治疗半阉割成年雌性大鼠,可减少卵巢代偿性肥大(OCH),并阻止己烯雌酚对OCH的抑制作用。双硫仑(多巴胺-β-羟化酶抑制剂)增强了己烯雌酚对OCH的抑制作用。小剂量左旋多巴刺激OCH,高剂量左旋多巴和苯妥英钠对ACH无作用,但增强了雌激素诱导的OCH抑制作用。提示促卵泡激素(FSH)的分泌是由中枢肾上腺素能神经元中去甲肾上腺素的释放介导的,而雌激素抑制FSH分泌的作用是通过刺激多巴胺释放介导的。

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