DIFFERENTIAL CARDIAC RESPONSES INDUCED BY NICOTINE SENSITIVE CANINE ATRIAL AND VENTRICULAR NEURONS

Objective: The aim was to study the locations and functions of atrial and ventricular nicotine sensitive neurones. Methods: In anaesthetised open chest dogs, cardiovascular effects elicited by nicotine (100 mug in 0.1 ml 0.9% saline), administered at specific loci of in situ atri al and ventricular ganglionated plexi, were studied before and after d ecentralisation. Results: Cardiovascular responses were elicited when 41% of atrial and 36% of ventricular ganglionated plexus loci were stu died. Subsequently, ganglia were identified adjacent to active sites. When cardiovascular responses were elicited, either tachycardia or bra dycardia was induced, depending on the locus investigated. When tachyc ardia occurred, atrial and/or ventricular forces were augmented. When bradycardia occurred, atrial forces were suppressed. Ventricular fibri llation was induced in two animals when ventricular ganglionated plexu s loci were investigated. Cardiovascular responses were not elicited w hen up to 2000 mug of nicotine were administered adjacent to intrinsic cardiac axons, indicating that responses were not primarily due to ax onal effects. Control injections of saline (0.1 ml) into active loci d id not elicit cardiovascular responses. Following acute decentralisati on, responses initiated by nicotine were attenuated or eliminated. Dep ressor responses were no longer elicited following atropine administra tion, nor augmentor ones following propranolol administration. Conclus ions: (1) The canine heart contains nicotine sensitive neurones which can induce either augmentor or depressor cardiac effects. (2) Nicotine sensitive atrial neurones modify primarily, but not exclusively, atri al tissues, whereas ventricular ones modify primarily, but not exclusi vely, ventricular tissues. (3) Nicotine sensitive intrinsic cardiac ne urones can interact with central neurones to modulate the heart.