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在麻醉大鼠中脑池内注射卡巴胆碱的中枢介导心血管效应。

Centrally mediated cardiovascular effects of intracisternal application of carbachol in anesthetized rats.

作者信息

Ozawa H, Uematsu T

出版信息

Jpn J Pharmacol. 1976 Jun;26(3):339-46. doi: 10.1254/jjp.26.339.

Abstract

The pressor response to the intracisternal (i.c.) injection of carbachol (1 mug) in anesthetized rats was analyzed. This response was significantly reduced by the intravenous (i.v.) injection of guanethidine (5 mg), hexamethonium (10 mg) or phentolamine (5 mg), and conversely, potentiated by i.v. desmethylimipramine (0.3 mg), while propranolol (0.5 mg) i.v. selectively inhibited the enlargement of pulse pressure and the tachycardia following i.c. carbachol (1 mug). On the other hand, the pressor response to i.c. carbachol (1 mug) was almost completely blocked by i.c. atropine (3 mug) or hexamethonium (500 mug), and significantly reduced by i.c. chlorpromazine (50 mug) but significantly potentiated by i.c. desmethylimipramine (30 mug). The pressor response to i.c. carbachol (1 mug) remained unchanged after sectioning of the bilateral cervical vagal nerves but disappeared after sectioning of the spinal cord (C7-C8). From the above result it is suggested that the pressor response to i.c. carbachol ortral and peripheral adrenergic mechanisms, and that the sympathetic trunk is the main pathway.

摘要

分析了麻醉大鼠脑池内注射卡巴胆碱(1微克)后的升压反应。静脉注射胍乙啶(5毫克)、六甲铵(10毫克)或酚妥拉明(5毫克)可显著降低该反应,相反,静脉注射去甲丙咪嗪(0.3毫克)可增强该反应,而静脉注射普萘洛尔(0.5毫克)可选择性抑制脑池内注射卡巴胆碱(1微克)后脉压增大和心动过速。另一方面,脑池内注射阿托品(3微克)或六甲铵(500微克)几乎完全阻断了对脑池内注射卡巴胆碱(1微克)的升压反应,脑池内注射氯丙嗪(50微克)可显著降低该反应,但脑池内注射去甲丙咪嗪(30微克)可显著增强该反应。双侧颈迷走神经切断后,对脑池内注射卡巴胆碱(1微克)的升压反应保持不变,但脊髓(C7-C8)切断后该反应消失。从上述结果表明,对脑池内注射卡巴胆碱的升压反应涉及中枢和外周肾上腺素能机制,且交感干是主要途径。

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