Vagal stimulation induces complex, phasic changes in the pacemaker cycle length of the sinus node depending on the timing and duration of the induced hyperpolarization.
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No immediate clinical implications for sinus node modulation; hypothesis-generating for phasic vagal effects in vivo.
We studied the functional interactions between the sinoatrial (SA) nodal pacemaker and the vagus nerve in isolated right atrium-vagus nerve preparations of the kitten. Brief trains of stimuli applied to the vagus nerve scanning the spontaneous pacemaker cycle induce a brief hyperpolarization of the membrane of cells in the pacemaker region. Aa a result of this hyperpolarization, there occur phasic changes in pacemaker cycle length that depend on the timing, amplitude, and duration of the hyperpolarization and, also, on the relationship between the duration of the hyperpolarization and the pacemaker cycle length. If the duration of the hyperpolarization is long relative to the duration of the spontaneous cycle, the next discharge can be delayed but not accelerated, no matter when during the cycle vagal stimuli are applied. If the duration of the hyperpolarization is briefer than the spontaneous cycle and the vagal input is presented early in the cycle, a postinhibitory rebound accelerates the next discharge. These effects of the vagal burst on the pacemaker cycle can be described by an inhibitory curve consisting of several components: a latent period of about 200 msec, a phase of major prolongation of the first and sometimes the second pacemaker cycle, a phase of relative or actual acceleration, and a final phase of lesser deceleration lasting several seconds. These effects can be approximated closely in a sucrose gap preparation of the sinus node by brief hyperpolarizing current pulses spanning the spontaneous pacemaker cycle in the test compartment.
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Jalife et al. (1979) studied this question.
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