Wendt D J, Martins J B
Department of Internal Medicine, University of Iowa College of Medicine, Iowa City 52242.
Am J Physiol. 1990 May;258(5 Pt 2):H1420-6. doi: 10.1152/ajpheart.1990.258.5.H1420.
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.
为了在体内表征自主神经系统对浦肯野系统的影响，我们测量了浦肯野相对不应期（PRRP）对交感神经（SNS）和迷走神经刺激（VNS）的反应。SNS对PRRP的影响主要通过β-肾上腺素能机制介导，因为在SNS期间PRRP缩短[从215±7（SE）至202±8毫秒，P<0.01]完全被美托洛尔（1毫克/千克）阻断。在安静状态下，即使相邻肌肉的有效不应期延长，迷走神经的影响也不会延长PRRP。当用毒扁豆碱增强VNS时，PRRP从205±12延长至212±13毫秒，P<0.05。当在SNS期间进行VNS时，对PRRP发生了类似的副交感神经效应激发；PRRP从188±9延长至193±9毫秒，P<0.05。此外，当在美托洛尔（1毫克/千克）存在下通过苯肾上腺素输注（25微克·千克-1·分钟-1）产生α-肾上腺素能刺激时，PRRP从242±8延长至246±9毫秒，P<0.05，加入VNS进一步将PRRP从246±9延长至253±9毫秒，P<0.05。因此，浦肯野系统中的一些不应期反应与相邻肌肉相似，因为β-肾上腺素能激活缩短了不应期，而迷走神经刺激拮抗了这种缩短。浦肯野组织特有的发现是，当α-肾上腺素能刺激期间不应期同时延长而促进迷走神经刺激时，不应期延长。
