Atrial ectopic pacemaker escape mediated by phasic vagal nerve activity.

Effects of vagal nerve activity on atrial ectopic pacemaker foci were studied in vitro in strips of rabbit tricuspid valve. Transmembrane potentials were recorded from pacemaker and working atrial fibers superfused with Tyrode solution containing propranolol. Tissues were paced from the atrial muscle end at cycle lengths of 90, 70, or 50% of the intrinsic pacemaker cycle, and postganglionic vagal nerve endings were stimulated with brief trains of pulses (200 Hz; 100-200 microseconds) through a second electrode near the pacemaker. Vagal trains scanning diastole hyperpolarized pacemaker and surrounding fibers to a maximum membrane potential of -74.7 +/- 1.8 mV (normal maximum diastolic potential = -75.5 +/- 1.6 mV) and elicited a period of inexcitability lasting 217.9 +/- 27.3 ms (drive cycle = 90% of pacemaker cycle). Inexcitability was evident at critical diastolic intervals where vagal input prevented atrial impulses from activating the pacemaker allowing spontaneous discharges to occur, i.e., escape, late in diastole. Besides inexcitability, incidence and timing of escape impulses were determined by cumulative effects of drive cycle length, vagal stimulus, and subthreshold electrotonic input on intrinsic pacemaker cycle. These data suggest that phasic vagal stimuli may transiently protect atrial ectopic pacemaker foci from conducted sinus impulses by rendering pacemaker and surrounding fibers inexcitable. In the setting of a long sinus (drive) cycle length, phasic vagal activity may result in spontaneous discharges manifest as late atrial premature beats.