Runge M, Luckmann E, Narula O S
Basic Res Cardiol. 1976 Nov-Dec;71(6):565-87.
32 patients were studied by His-bundle recordings to examine the extent to which frequency and autonomic nervous system influence the conduction velocity in the subdivisions (atrium, AV-node, His-Purkinje system) of the normal PR-interval. The measurements were performed during sinus rhythm and three electrically induced atrial frequencies before and after intravenous administration of 1 mg Atropine (15 patients) and 0.4 mg Visken (17 patients). In influencing the atrial conduction velocity frequency dominates the blockade of both components of the autonomic nervous system. Increase in frequency lengthens the intraatrial conduction time. Blockade of parasympathicus and sympathicus does not significantly influence the changes in intraatrial conduction velocity induced by increase of frequency. Patients with prolonged intraatrial conduction respond in the same way to cycle length shortening and blockade of the autonomic tone as patients with normal conduction. The results are discussed with respect to acetylcholine and catecholamine influence on the electrophysiological properties of the atrial myocardium. The AV-node is the part of the conduction system most sensitive to the influence of both cycle length shortening and blockade of the autonomic nervous system. Artificially induced cycle length shortening prolongs the intranodal conduction time to a different individual level for each patient. Blockade of the parasympathicus not only shortens this interval but also reduces the steepness of the AH-time induced by atrial pacing. Blockade of the sympathicus has the opposite effect. The most likely explanation for these results is the abolishing of the functional dissociation within the AV-node by blocking the autonomic influence on this structure. The conduction velocity in the His-Purkinje system is influenced neither by atrial pacing nor by blockade of both components of the autonomic nervous system.
对32例患者进行希氏束记录研究,以考察频率和自主神经系统对正常PR间期各细分部分(心房、房室结、希氏-浦肯野系统)传导速度的影响程度。测量在窦性心律期间以及静脉注射1毫克阿托品(15例患者)和0.4毫克哌唑嗪(17例患者)前后的三种电诱发心房频率下进行。在影响心房传导速度方面,频率起主导作用,自主神经系统的两个分支均被阻断。频率增加会延长心房内传导时间。阻断副交感神经和交感神经对频率增加引起的心房内传导速度变化无显著影响。心房内传导延长的患者对周期长度缩短和自主神经张力阻断的反应与传导正常的患者相同。就乙酰胆碱和儿茶酚胺对心房心肌电生理特性的影响对结果进行了讨论。房室结是传导系统中对周期长度缩短和自主神经系统阻断影响最敏感的部分。人为诱发的周期长度缩短会使每个患者的结内传导时间延长到不同的个体水平。阻断副交感神经不仅会缩短该间期,还会降低心房起搏诱发的AH间期的斜率。阻断交感神经则有相反的效果。这些结果最可能的解释是通过阻断自主神经对该结构的影响,消除了房室结内的功能解离。希氏-浦肯野系统的传导速度既不受心房起搏影响,也不受自主神经系统两个分支阻断的影响。