Effects Of Nicotine On Electrophysiology Of Atrioventricular Node And Underlying Mechanisms

Object: Smoking is harmful to health and it can induce many cardiac diseases. Nicotine is the main component of tobacco and it could elevates plasma catecholamines,heart rate and arterial blood pressure; produces coronary spasm and increases myocardial work and oxygen demand with concomitant reduction in oxygen supply.　This may increase the morbidity of the coronary diseases and an incidence of sudden death.　 Mehta MC et al.　reported that nicotion could induced many kinds of cardiac arrhythmias which included sinus arrest, atrial flutter, atrial fibrillation, bradycardia, first-degree and second-degree heart block, atrioventricular dissociation, ventricular premature, bigeminy, ventricular flutter, ventricular fibrillation and so on. Reserchers have done a lot of work in effects of nicotine on electrophysiology of cardiomyocytes for many years, most of which is about atria ,ventricle and sino-atrial node, till now little is know about effects of nicotine on electrophysiology of atrioventricular node. In order to study the effect of nicotine on electrophysiology of atrioventricular node and make clear the relationship bweteen it and atrioventricular arrhythmias, the present work was undertaken to study theeffect of nicotine on elecphysiology of the rabbit atrioventricular node with intracellular microelectrode technique and underlying mechanism.Method: Rabbits were stunned by heavy blow on the heads and the hea1rts were quickly excised which were put into the Tyrode solution (0-4oC).The atrioventricular node was dissected from the heart and put into perfusion chamber superfused with Tyrode solution (36±0.5oC) continuously saturated with a mixture of 95%O2 and 5%CO2. Transmembrance action potentials were recorded from spontaneous cells of atrioventricular node with a glass microelectrode filled with KCl 3mol/L (a tip resistance of 10-20MΩ),coupled to a high input impedence amplifier. The amplified signals were fed to the A/D convertor and processed by a microcomputer. Drugs used in this study were dissolved in Tyrode solution which was superfused into perfused chamber and effects of drugs on parameters of action potential of atrioventricular node were recorded. Results: (1) Nicotine (12 μmol/L) has no effect on atrioventricular node cells. Nicotine (60μmol/L) has negative and slight trasient positive effects on RSF of atrioventricular node autonomic cells and nicotine of high concentration (300μmol/L 600μmol/L)has negative and obvious trasient positive effects on RSF of atrioventricular node cells. (2) The trasient positive effect of nicotine (300μmol/L) could be blocked completely by pretreatmentwith propanolol (4μmol/L) (3) The negative effect of nicotine (300μmol/L) could be blocked completely by pretreatment with atropine (10μmol/L) (4) Nicotine of high concentration could prolong action potential duration of atrioventricular node cells. (5) After pretreatment with propanolol (4μmol/L) and atropine (10μmol/L), nicotine of high concentration could prolong action potential duration of atrioventricular node cells. Conclusion: (1) Nicotine could induce negative and trasient positive effects on RSF of atrioventricular node cells propably mediated by parasympathetic ganglionic nicotinic receptors and presynaptic nicotinic receptors of the postganglionic sympathetic nerves. (2) nicotine of high concentration could prolong action potential duration afterβ-receptors and M-receptors were blocked...