Key result
In parasympathetically denervated dog hearts, intense vagus stimulation during sympathetic stimulation shifted the earliest activation site to the SA node or inferior pacemaker region in 15 of 18 experiments.
In parasympathetically denervated dog hearts, activation of parasympathetic elements outside the SA fat pad attenuates sympathetically-evoked increases in heart rate and shifts in pacemaker location via pre- and postsynaptic interactions.
Does not support clinical autonomic interventions; leaves open whether parasympathetic-sympathetic interactions translate to intact human hearts.
INTRODUCTION: Parasympathetic activity predominates over sympathetic activity not only with respect to heart rate but also with respect to the pacemaker location in the dog heart. After we removed the parasympathetic neural elements in the sinoatrial (SA) fat pad in the right atrium, we observed that cervical vagus stimulation did not decrease the atrial rate, but it did suppress the increase in rate evoked by sympathetic stimulation. We determined whether the pacemaker rate and location were affected by presynaptic or postsynaptic mechanisms. METHODS AND RESULTS: We determined the earliest activation site by means of isochronic activation mapping of the right atrium of open chest, anesthetized dog hearts. An electrode array, which consisted of 48 unipolar electrodes, was used to record atrial activation. This array covered the three main pacemaker regions, including the SA node region. After parasympathetic nerve fibers in the SA fat pad had been denervated, vagus stimulation at 10 and 30 Hz did not decrease the heart rate, but it attenuated the increase in heart rate evoked by sympathetic stimulation or isoproterenol. Vagus stimulation at 10 Hz during sympathetic stimulation did not shift the earliest activation site from the superior pacemaker region to the SA node region in 11 of 18 experiments. However, vagus stimulation at 10 Hz during isoproterenol infusion shifted the earliest activation site to the SA node region in 11 of 13 experiments. More intense vagus stimulation during combined sympathetic stimulation or isoproterenol infusion shifted the earliest activation site to the SA node or the inferior pacemaker region in 15 of 18 and in all experiments, respectively. CONCLUSION: The results suggest that activation of parasympathetic elements not located in the SA fat pad attenuates the increase in heart rate and the shift in pacemaker location evoked by sympathetic activation. The sympathetic and parasympathetic effects interact at presynaptic and postsynaptic sites in the dog heart.
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Nakajima et al. (2002) studied Parasympathetically denervated dog hearts (n=18). Vagus stimulation vs. Sympathetic stimulation or isoproterenol alone was evaluated on Shift in earliest activation site and heart rate. In parasympathetically denervated dog hearts, intense vagus stimulation during sympathetic stimulation shifted the earliest activation site to the SA node or inferior pacemaker region in 15 of 18 experiments.
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