Functional capacity of nicotine-sensitive canine intrinsic cardiac neurons to modify the heart.

The capacity of intrinsic cardiac efferent parasympathetic and sympathetic neurons to modify the heart was investigated in nine anesthetized open-chest dogs with adrenal glands removed from the circulation. The effects elicited by intravenously administered isoproterenol, tyramine, and nicotine on cardiac variables were examined before and after acute decentralization of the heart. Major vessels, as well as other tissues at the base of the heart, were denuded by means of an ultrasonic aspirator that removed neural elements without damaging muscles or blood vessels. The efficacy of the acute decentralization was assured by testing cardiac responses elicited by right and left stellate ganglia and cervical vagosympathetic complex stimulations after surgery. Heart rate, atrial force, and both right and left ventricular intramyocardial systolic pressures were augmented similarly by isoproterenol and tyramine before and after acute decentralization, indicating that the surgery necessary to decentralize the heart did not obtund cardiac myocyte function. Power spectral analysis of heart rate and left ventricular chamber pressure rate of change indicated an almost complete lack of variability of these indexes after, but not before, acute decentralization. Despite these changes, similar cardiac augmentation was elicited by nicotine before and after acute decentralization. Cardiac augmentation was elicited by nicotine in acutely decentralized preparations after atropine administration but not after beta-adrenergic blockade. These data indicate that the canine intrinsic cardiac nervous system contains a significant population of nicotine-sensitive adrenergic neurons that modulate the heart. Furthermore, the intrinsic cardiac nervous system does not appear to be primarily responsible for the heart rate and ventricular pressure variability found in intact hearts.