窦主动脉去神经的中枢胆碱能刺激。脑室内给药拟胆碱剂的作用[j]。

C A Taira
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引用次数: 0

摘要

通过分析几种毒蕈碱类激动剂和抗胆碱酯酶新斯的明经静脉或脑室内给药的心血管作用,决定对胆碱能参与窦主动脉去神经支配实验模型进行药理学研究。脑内注射新斯的明后,还对中枢神经系统不同结构的乙酰胆碱酯酶活性进行了评估。窦主动脉去神经支配增加了心室灌注激动剂比萘酚和抗胆碱酯酶新斯的明的降压反应,但减少了心动过缓的作用。然而,它不会改变静脉注射激动剂oxotremorine和静脉注射激动剂McNeil-A-343的心血管反应。新斯的明1次给药后,下丘脑组织酶活性在24% ~ 30%之间波动,其余组织在42% ~ 52%之间波动,假手术大鼠与窦主动脉去神经组无差异。结果表明,毒蕈碱受体M亚型不参与中枢胆碱能刺激的心血管效应,另一方面,它支持毒蕈碱受体参与观察到的变化的观点。由于采用新斯的明给药方式,观察到下丘脑乙酰胆碱酯酶的抑制程度更大,提示下丘脑结构可能参与了脑内给药引起的心血管效应。
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[The central cholinergic stimulation in sinoaortic denervation. Effect of intracerebroventricular administration of cholinomimetic agents].

It was decided to made a pharmacological study of the cholinergic participation in the sinoaortic denervation experimental model by analyzing the cardiovascular effects of several muscarinic agonists and the anticholinesterase neostigmine administered either by intravenous via or by the intracerebroventricular via. The activity of the enzyme acetylcholinesterase was also evaluated in diverse structures of the central nervous system after the intracerebral administration of neostigmine. Sinoaortic denervation increases the pressor response to the i.c.v. administration of the agonist bethanechol and of the anticholinesterase neostigmine but it diminishes the bradycardic effect. However it would not alter the cardiovascular responses to the i.v. injection of the agonist oxotremorine and to the i c v. administration of the agonist McNeil-A-343. After the i c v. administration of neostigmine, the enzymatic activity oscillated among 24%-30% in hypothalamic structures and among 42%-52% in the remaining tissues, without differences between the rats with sham operation and those with sinoaortic denervation. The results suggest that M, muscarinic receptor subtype would not be involved in the cardiovascular effects of the central cholinergic stimulation On the other hand, it would support the idea of an involvement of muscarinic receptors in the observed changes. Because the used route of administration of neostigmine, a greater degree of inhibition of the hypothalamic acetylcholinesterase is observed, suggesting then that the hypothalamic structures could be involved in the cardiovascular effects induced by the intracerebral administration of the anticholinesterase.

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