Region in Anesthetized Dogs

We gave atropine intravenously to autonomically decentralized, open-chest, anesthetized dogs and stimulated the discrete intracardiac sympathetic nerve fibers to the sinoatrial (SA) (SAS stimulation) or atrioventricular (AV) (AVS stimulation) nodal region. A brief burst of neural stimuli was delivered during each cardiac cycle. SAS stimulation consistently decreased the atrial cycle length but had variable effects on the AV interval. The positive chronotropic response to SAS stimulation increased when the level of stimulation (i.e., stimulus pulse duration, pulse amplitude, and number of pulses per burst) was increased. When the heart rate was held constant by atrial pacing, SAS stimulation did not change the AV interval. AVS stimulation decreased the AV conduction time but did not change the atrial cycle length. The AV conduction response increased when the level ofAVS stimulation was increased. A high level of AVS stimulation induced an AV junctional rhythm in seven of eight experiments. When the atrial pacing interval was decreased, the basal AV interval increased, and the decrease in AV interval induced by AVS stimulation was exaggerated. The chronotropic response to SAS stimulation and the dromotropic response to AVS stimulation were abolished by propranolol given systemically and by lidocaine given topically. From these results, we conclude that in anesthetized dogs treated with atropine, activation of the discrete intracardiac sympathetic nerves to the SA and AV nodal regions controls the sinus rate and AV conduction time independently and activation of the discrete sympathetic nerves may shift the dominant pacemaker site to a subsidiary site. (Circulation Research 1990;66:1391-1399)