Differential cardiac responses induced by nicotine sensitive canine atrial and ventricular neurones.

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 micrograms in 0.1 ml 0.9% saline), administered at specific loci of in situ atrial and ventricular ganglionated plexi, were studied before and after decentralisation.
RESULTS: Cardiovascular responses were elicited when 41% of atrial and 36% of ventricular ganglionated plexus loci were studied. Subsequently, ganglia were identified adjacent to active sites. When cardiovascular responses were elicited, either tachycardia or bradycardia was induced, depending on the locus investigated. When tachycardia occurred, atrial and/or ventricular forces were augmented. When bradycardia occurred, atrial forces were suppressed. Ventricular fibrillation was induced in two animals when ventricular ganglionated plexus loci were investigated. Cardiovascular responses were not elicited when up to 2000 micrograms of nicotine were administered adjacent to intrinsic cardiac axons, indicating that responses were not primarily due to axonal effects. Control injections of saline (0.1 ml) into active loci did not elicit cardiovascular responses. Following acute decentralisation, responses initiated by nicotine were attenuated or eliminated. Depressor responses were no longer elicited following atropine administration, nor augmentor ones following propranolol administration.
CONCLUSIONS: (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, atrial tissues, whereas ventricular ones modify primarily, but not exclusively, ventricular tissues. (3) Nicotine sensitive intrinsic cardiac neurones can interact with central neurones to modulate the heart.