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关于超敏化的药理学研究。IX. 曲吡那敏、N,N-二甲基-N',N'-二苄基乙二胺和N,N-二苄基-N',N'-二甲基-1,2-丙二胺诱导的豚鼠输精管非特异性超敏反应

Pharmacological studies on supersensitization. IX. Non-specific supersensitivity of vas deferens of guinea pig induced by tripelennamine, N,N-dimethyl-N',N'-dibenzylethylenediamine and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine.

作者信息

Araki K, Ohashi T, Gomi Y

出版信息

J Pharmacobiodyn. 1982 Nov;5(11):905-10. doi: 10.1248/bpb1978.5.905.

Abstract

Effects of tripelennamine, N,N-dimethyl-N',N'-dibenzylethylenediamine (DBED) and N,N-dibenzyl-N',N'-dimethyl-1,2-propanediamine (DBPD) on the isotonic contractions of isolated vas deferens of guinea pig were examined. These ethylenediamines, except DBPD, induced slight but significant increase in sensitivity of vas deferens to K+. Tripelennamine induced dose-dependent potentiation to epinephrine and norepinephrine, but tripelennamine-induced augmentation of acetylcholine-contractions was weak and dose-independent. DBED potentiated both catecholamines and acetylcholine in a dose-dependent way and in the same degree. The degree of DBPD-induced augmentation of epinephrine- and norepinephrine-induced contractions was dose-independent and much weaker than that of acetylcholine-contractions. Tripelennamine and DBED did not affect the contractile response to tyramine, while DBPD potentiated the contractile response to tyramine. These results suggest the following possibilities: 1) tripelennamine affects both amine uptake mechanism and beyond receptor mechanism of contractile processes and induced supersensitivity of various stimulants. 2) DBED affects mainly beyond receptor mechanism of contractile processes and augments the contractile responses to various stimulants. 3) The mechanism of DBPD-induced supersensitivity remained obscure, but the inhibition of the metabolic degradation of stimulants was proposed as one of the possible mechanism of supersensitization.

摘要

研究了曲吡那敏、N,N-二甲基-N',N'-二苄基乙二胺(DBED)和N,N-二苄基-N',N'-二甲基-1,2-丙二胺(DBPD)对豚鼠离体输精管等张收缩的影响。除DBPD外,这些乙二胺均能使输精管对K+的敏感性轻微但显著增加。曲吡那敏对肾上腺素和去甲肾上腺素诱导剂量依赖性增强作用,但曲吡那敏对乙酰胆碱收缩的增强作用较弱且与剂量无关。DBED以剂量依赖性方式且程度相同地增强儿茶酚胺和乙酰胆碱的作用。DBPD对肾上腺素和去甲肾上腺素诱导的收缩增强程度与剂量无关,且远弱于对乙酰胆碱收缩的增强程度。曲吡那敏和DBED不影响对酪胺的收缩反应,而DBPD增强对酪胺的收缩反应。这些结果提示以下可能性:1)曲吡那敏影响胺摄取机制及收缩过程的受体后机制,并诱导各种刺激物超敏反应。2)DBED主要影响收缩过程的受体后机制,并增强对各种刺激物的收缩反应。3)DBPD诱导超敏反应的机制尚不清楚,但推测刺激物代谢降解的抑制是超敏化的可能机制之一。

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