FUNCTIONAL-CAPACITY OF NICOTINE-SENSITIVE CANINE INTRINSIC CARDIAC NEURONS TO MODIFY THE HEART

The capacity of intrinsic cardiac efferent parasympathetic and sympath etic 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, tyramin e, and nicotine on cardiac variables were examined before and after ac ute decentralization of the heart. Major vessels, as well as other tis sues at the base of the heart, were denuded by means of an ultrasonic aspirator that removed neural elements without damaging muscles or blo od 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 intramyocardi al systolic pressures were augmented similarly by isoproterenol and ty ramine before and after acute decentralization, indicating that the su rgery necessary to decentralize the heart did not obtund cardiac myocy te function. Power spectral analysis of heart rate and left ventricula r chamber pressure rate of change indicated an almost complete lack of variability of these indexes after, but not before, acute decentraliz ation. Despite these changes, similar cardiac augmentation was elicite d by nicotine before and after acute decentralization. Cardiac augment ation was elicited by nicotine in acutely decentralized preparations a fter atropine administration but not after beta-adrenergic blockade. T hese data indicate that the canine intrinsic cardiac nervous system co ntains a significant population of nicotine-sensitive adrenergic neuro ns 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.