可卡因及慢性交感神经去神经支配对迷走神经逃逸的作用

Action of cocaine and chronic sympathetic denervation on vagal escape.

作者信息

Campos H A, Urquilla P R

出版信息

J Physiol. 1969 Feb;200(2):311-20. doi: 10.1113/jphysiol.1969.sp008695.

DOI:10.1113/jphysiol.1969.sp008695

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1350469/

Abstract

The effect of cocaine has been studied on vagal escape and on the tachycardia due to vagal stimulation in the atropinized dog. All the dogs were submitted to acute cervical section of the spinal cord and acute or chronic sympathetic denervation.2. Cocaine, 5 mg/kg or 40 mug/kg/min, I.V., induces a significant enhancement of the ventricular escape. The effects of a continuous infusion of cocaine are more reproducible than those of a single injection of the drug.3. Cocaine, 40 mug/kg/min, I.V., potentiates the tachycardia due to vagal stimulation in the atropinized dog.4. Chronic thoracic sympathectomy markedly retards the recovery of the ventricular rate from the inhibitory action of the vagus. Under this condition, the infusion of cocaine does not significantly enhance the ventricular escape.5. These findings suggest that an adrenergic mechanism located at the sympathetic nerves supplying the heart is substantially involved in the phenomenon of vagal escape.

摘要

已经研究了可卡因对阿托品化犬的迷走神经脱逸以及迷走神经刺激所致心动过速的影响。所有犬均接受了脊髓急性颈段切断术以及急性或慢性交感神经去神经支配。
静脉注射5毫克/千克或40微克/千克/分钟的可卡因可显著增强心室脱逸。持续输注可卡因的效果比单次注射该药物的效果更具可重复性。
静脉注射40微克/千克/分钟的可卡因可增强阿托品化犬因迷走神经刺激所致的心动过速。
慢性胸段交感神经切除术显著延缓了心室率从迷走神经抑制作用中的恢复。在这种情况下，输注可卡因不会显著增强心室脱逸。
这些发现表明，供应心脏的交感神经处的肾上腺素能机制在很大程度上参与了迷走神经脱逸现象。