In the intact canine Purkinje system, beta-adrenergic activation shortens the refractory period while vagal stimulation antagonizes this shortening and uniquely prolongs the refractory period when facilitated by alpha-adrenergic stimulation.
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Hypothesis-generating for autonomic modulation of Purkinje refractoriness; leaves open translation to human ventricular arrhythmias.
To characterize autonomic influences on the Purkinje system in vivo, we measured Purkinje relative refractory period (PRRP) in response to sympathetic (SNS) and vagal nerve stimulation (VNS). Effects of SNS on PRRP were primarily mediated via beta-adrenergic mechanisms because shortening of PRRP during SNS [from 215 +/- 7 (SE) to 202 +/- 8 ms, P less than 0.01] was entirely blocked by metoprolol (1 mg/kg). Vagal influences in the ambient state did not prolong PRRP, even when effective refractory period of adjacent muscle did prolong. When VNS was augmented with physostigmine, PRRP prolonged from 205 +/- 12 to 212 +/- 13 ms, P less than 0.05. Similar provocation of parasympathetic effects on PRRP occurred when VNS was performed during SNS; PRRP prolonged from 188 +/- 9 to 193 +/- 9 ms, P less than 0.05. Also, when alpha-adrenergic stimulation was produced by phenylephrine infusion (25 micrograms.kg-1.min-1) in the presence of metoprolol (1 mg/kg), which prolonged PRRP from 242 +/- 8 to 246 +/- 9 ms, P less than 0.05, the addition of VNS further prolonged PRRP from 246 +/- 9 to 253 +/- 9 ms, P less than 0.05. Thus some refractory period responses in the Purkinje system were similar to adjacent muscle, because beta-adrenergic activation shortened refractory period and vagal stimulation antagonized the shortening. Findings unique to Purkinje tissue were refractory period prolongation by vagal stimulation when facilitated by concurrent prolongation of refractory period during alpha-adrenergic stimulation.
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Wendt et al. (1990) studied this question.
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