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Effects of brief vagal bursting on pacemaker periodicity and intranodal conduction were studied by recording transmembrane potentials in isolated rabbit sinoatrial preparations. Postganglionic vagal terminals were activated by applying brief (50- to 150-msec) trains of pulses (duration, 100 mu sec; frequency, 200 Hz) to the endocardial surface of the node. Sympathetic effects were prevented by superfusion with Tyrode's solution containing propranolol (1 microgram/ml). Vagal trains applied singly every 10 seconds produced brief hyperpolarizations in "true" pacemaker and transitional cells, and induced phasic changes in periodicity and conduction. These changes were out of phase with each other, and were dependent on the magnitude and duration of the vagal train, as well as on its position within the pacemaker period. When similar trains were applied repetitively at cycle lengths (200-1200 msec) that were independent of the pacemaker period, complex patterns of vagus-sinoatrial node interactions resulted. Hence, depending on the vagal stimulus cycle length, the sinoatrial pacemaker was forced to beat at stable and predictable harmonic (i.e., 1:1, 1:2, 2:1, etc.), subharmonic (3:2, 4:3, etc.), or more complex entrainment ratios. At some of these ratios, arrhythmic sinus patterns coexisted with intranodal conduction disturbances, including first- and second-degree block, Wenckebach phenomena, or combinations thereof. At other entrainment ratios, arrhythmias occurred in the absence of conduction changes. At still other ratios, conduction disturbances developed in the presence of apparently undisturbed sinus rhythm. These results provide insight into the mechanism of the dynamic vagal control of sinoatrial periodicity and conduction, and may have clinical implications as well.

Vagal control of pacemaker periodicity and intranodal conduction in the rabbit sinoatrial node.