Sadr-Ameli M A, Shenasa M, Lacombe P, Faugère G, Nadeau R
Clinical Electrophysiology Laboratory, Sacré-Coeur Hospital, Montreal, Quebec, Canada.
Cardiovasc Res. 1987 Jan;21(1):45-54. doi: 10.1093/cvr/21.1.45.
Although the influence of the autonomic nervous system on anterograde atrioventricular nodal conduction is well established, its effect on retrograde atrioventricular nodal conduction has not been examined systematically. Since retrograde atrioventricular nodal conduction in subjects with normal anterograde conduction may vary from intact retrograde conduction to complete retrograde block when assessed during ventricular pacing, in this study patients with (a) intact retrograde atrioventricular nodal conduction (group 1) were studied during parasympathetic (vagal) stimulation by carotid sinus pressure and during sympathetic inhibition (propranolol 0.2 mg.kg-1 intravenously) and (b) retrograde atrioventricular nodal block (group 2) were studied during vagal blockade (atropine 0.04 mg.kg-1 intravenously) and during sympathetic stimulation (isoproterenol 1-4 micrograms.min-1 infusion). In both groups changes in sinus cycle length and anterograde atrioventricular nodal conduction were measured. In group 1 vagal stimulation by carotid sinus pressure in 20 patients caused the cycle length at which retrograde atrioventricular nodal block was induced to be significantly lengthened from a mean(SD) of 375(59) to 451(51) ms in six patients; caused complete retrograde block in 10 patients; and had no effect in four patients. Sympathetic inhibition by propranolol in another 15 patients delayed the onset of pacing induced retrograde atrioventricular nodal block from a mean(SD) of 340(60) to 418(80) ms in 11 patients; caused complete retrograde atrioventricular nodal block in three patients; and had no effect in one patient. In group 2 vagal blockade by atropine caused a 1:1 retrograde response during ventricular pacing up to a mean(SD) cycle length of 470(135) ms in six out of eight patients. The infusion of isoproterenol caused the retrograde atrioventricular nodal block to be abolished and 1:1 conduction to be resumed up to a ventricular pacing mean(SD) cycle length of 364(57) ms in six out of eight patients. It is concluded that (a) the autonomic nervous system modulates retrograde atrioventricular nodal conduction in a similar manner to its anterograde counterpart and (b) that since retrograde atrioventricular nodal conduction was reversible after the administration of either atropine or isoproterenol retrograde atrioventricular nodal block may be dynamic (physiological) rather than fixed (anatomical) in nature.
虽然自主神经系统对房室结前向传导的影响已得到充分证实,但其对房室结逆向传导的影响尚未得到系统研究。由于在心室起搏时评估,正常前向传导受试者的房室结逆向传导可能从完整的逆向传导到完全逆向阻滞不等,因此在本研究中,对(a)房室结逆向传导完整的患者(第1组)在通过颈动脉窦压力进行副交感神经(迷走神经)刺激期间以及交感神经抑制期间(静脉注射普萘洛尔0.2mg/kg)进行了研究,以及对(b)房室结逆向阻滞的患者(第2组)在迷走神经阻滞期间(静脉注射阿托品0.04mg/kg)以及交感神经刺激期间(静脉输注异丙肾上腺素1 - 4μg/min)进行了研究。在两组中均测量了窦性周期长度和房室结前向传导的变化。在第1组中,20例患者通过颈动脉窦压力进行迷走神经刺激,使6例患者诱发房室结逆向阻滞的周期长度从平均(标准差)375(59)ms显著延长至451(51)ms;使10例患者出现完全逆向阻滞;对4例患者无影响。另外15例患者通过普萘洛尔进行交感神经抑制,使11例患者起搏诱发房室结逆向阻滞的起始时间从平均(标准差)340(60)ms延迟至418(80)ms;使3例患者出现完全房室结逆向阻滞;对1例患者无影响。在第2组中,8例患者中有6例通过阿托品进行迷走神经阻滞,在心室起搏至平均(标准差)周期长度470(135)ms期间导致1:1逆向反应。静脉输注异丙肾上腺素使8例患者中有6例的房室结逆向阻滞被消除,在心室起搏平均(标准差)周期长度364(57)ms期间恢复1:1传导。得出的结论是:(a)自主神经系统以与其前向传导类似的方式调节房室结逆向传导;(b)由于在给予阿托品或异丙肾上腺素后房室结逆向传导是可逆的,因此房室结逆向阻滞在本质上可能是动态的(生理性的)而非固定的(解剖性的)。