ARRHYTHMIA INDUCED BY NICOTINE ACTIVATING CARDIAC INTRINSIC NEURONS IN CANINE ATRIAL AND VENTRICULAR GANGLIAL PLEXUS  

作　　者：Yuan Bingxiang(袁秉祥) Liu Shuqin(刘书勤) Li Ping(李萍) Li Xinhua(李新华) 

机构地区：[1]Department of Pharmacology, Medical school of Xi''an Jiaotong University, Xi''an 710061, China. Department of Pharmacology, Medical school of Xi''an Jiaotong University, Xi''an 710061, China. Department of Pharmacology, Medical school of Xi''an Jiaotong University, Xi''an 710061, China. Department of Pharmacology, Medical school of Xi''an Jiaotong University, Xi''an 710061, China.

出　　处：《Academic Journal of Xi'an Jiaotong University》2002年第2期155-158,共4页西安交通大学学报（英文版）

基　　金：ThisworkwassupportedbytheNationalNatureScienceFoundationofChina (No .396 70 2 45 );theScience FoundationofChina’sHealthMinistry( 1996 6 6 ) .

摘　　要：Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ganglial plexus between aorta and pulmonary artery (A-PGP) in 33 anesthetized open-chest dog, electrocardiogram, atrial force and ventricular intramyocardial pressures (IMP) were recorded. The responses were also recorded following administration of atropine or propranolol and after heart acute decentralization. Results Ventricular arrhythmia (VA) was induced by injections of nicotine into A-PGP, but not by injections of nicotine into RAGP in 13 dogs. Atrioventricilar (A-V) block was induced by nicotine activating RAGP in 10 dogs, but not by nicotine activating A-PGP. Propranolol could reduce the frequency of VA elicited by stimulating A-PGP, atropine could reduce the frequency of A-V block elicited by stimulating RAGP. After acute decentralization, VA was still induced by activation of A-PGP in 9 dogs, but A-V block elicited by stimulating RAGP was decreased. Conclusion VA is induced by stimulating N receptor in cardiac nicotine-sensitive efferent sympathetic neurons of ventricular ganglial plexus (A-PGP), and then modifying β receptor of ventricles. A-V block is elicited by stimulating N receptor in atrial ganglial plexus (RAGP), then modifying M receptor of A-V node not only via efferent parasympathetic neurons, but also via afferent pathway.Objective To study the arrhythmia induced by stimulation of nicotine-sensitive neurons in cardiac ganglial plexuses. Methods When nicotine (100 μg ) was injected into canine right atrial ganglial plexus (RAGP) and ganglial plexus between aorta and pulmonary artery (A-PGP) in 33 anesthetized open-chest dog, electrocardiogram, atrial force and ventricular intramyocardial pressures (IMP) were recorded. The responses were also recorded following administration of atropine or propranolol and after heart acute decentralization. Results Ventricular arrhythmia (VA) was induced by injections of nicotine into A-PGP, but not by injections of nicotine into RAGP in 13 dogs. Atrioventricilar (A-V) block was induced by nicotine activating RAGP in 10 dogs, but not by nicotine activating A-PGP. Propranolol could reduce the frequency of VA elicited by stimulating A-PGP, atropine could reduce the frequency of A-V block elicited by stimulating RAGP. After acute decentralization, VA was still induced by activation of A-PGP in 9 dogs, but A-V block elicited by stimulating RAGP was decreased. Conclusion VA is induced by stimulating N receptor in cardiac nicotine-sensitive efferent sympathetic neurons of ventricular ganglial plexus (A-PGP), and then modifying β receptor of ventricles. A-V block is elicited by stimulating N receptor in atrial ganglial plexus (RAGP), then modifying M receptor of A-V node not only via efferent parasympathetic neurons, but also via afferent pathway.

关 键 词：NICOTINE ARRHYTHMIA ganglial plexuses efferent NEURONS AFFERENT NEURONS 

分 类 号：R972[医药卫生—药品]