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Parasympathetic pathways mediating chronotropic and dromotropic responses to cervical vagal stimulation were determined from sequential, restricted, intrapericardial dissection around major cardiac vessels. Although right cervical vagal input evoked significantly greater bradycardia, supramaximal electrical stimulation of either vagus produced similar ventricular rates, both with and without simultaneous atrial pacing. Dissection of the triangular fat pad at the junction of the inferior vena cava-inferior left atrium (IVC-ILA) invariably eliminated all vagal input to the atrioventricular (AV) nodal region. Yet IVC-ILA dissection had minimal influence on evoked-chronotropic responses to either cervical vagal or stellate ganglia stimulation. Respective intrapericardial projection pathways, from either right or left vagi, are sufficiently distinct to allow unilateral parasympathetic denervation of the sinoatrial (SA) and atrioventricular (AV) nodal regions. Left vagal projections to the SA and AV nodal regions course primarily along and between the right pulmonary artery and left superior pulmonary vein. Right vagal projections to the SA and AV nodal regions are somewhat more diffuse but concentrate around the right pulmonary vein complex and adjacent segments of the right pulmonary artery. We conclude there are parallel, yet functionally distinct, inputs from right and left vagi to the SA and AV nodal regions.

The purpose of this study was to quantify the relative roles of the canine cardiac parasympathetic and sympathetic nerves in controlling the distribution of power within the heart rate (HR) power spectrum using a highly selective surgical technique to parasympathectomize the SA node. DAta were recorded in awake dogs (n = 6) before and after the selective denervation; the animals were isolated from human contact and their behavior carefully monitored during the measurements. The average amplitude in the high-frequency (approximately 0.32 Hz) peak in the HR power spectrum decreased from a predenervation control of 2.68 +/- 1.54 (mean +/- SD, arbitrary units) to 0.07 +/- 0.06 (P less than 0.05). Corresponding resting HR increased from 80 +/- 9 to 106 +/- 16 beats/min (P less than 0.05). The low-frequency peak (approximately 0.02 Hz) also decreased from a control of 2.45 +/- 1.18 to a postparasympathectomy value of 1.25 +/- 0.92 (P less than 0.05). beta-Adrenergic blockade (propranolol, 1 mg/kg) further decreased the latter peak to 0.59 +/- 0.52 (P less than 0.05). These data directly demonstrate that the high-frequency peak of the HR power spectrum 1) results from parasympathetic control of SA nodal automaticity, while 2) the low-frequency peak reflects activity in both divisions of the autonomic nervous system.

The activity of 394 spontaneously active neurons located in the ganglionated plexus of the ventral epicardial fat pad overlying the right atrium and pulmonary veins was recorded. Ganglia that contained various numbers of neurons, many with two or more nucleoli, were identified adjacent to the recording sites. Spontaneous activity was correlated with the cardiac cycle in 39% and with the respiratory cycle in 8% of the identified neurons. Neuronal activity occurred in specific phases of the cardiac cycle when arterial pressure was between approximately 70 and 175 mmHg. During increases in systolic pressure induced by positive inotropic agents or aortic occlusion, responses of neurons that displayed cardiovascular-related activity were enhanced. These responses persisted after acute decentralization. The activity of 14% of all identified neurons was altered when discrete regions of the heart, great thoracic vessels, or lungs were mechanically distorted by gentle touch. Trains of stimuli, but not single stimuli, delivered to the vagosympathetic complexes, stellate ganglia, or cardiopulmonary nerves activated ganglionic neurons in intact or acutely decentralized preparations. It is concluded that the activity of some cardiac ganglion neurons is related to cardiovascular or respiratory dynamics and that some of these neurons receive inputs from sympathetic and parasympathetic efferent axons as well as from cardiac mechanoreceptors.

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