Morillo C A, Eckberg D L, Ellenbogen K A, Beightol L A, Hoag J B, Tahvanainen K U, Kuusela T A, Diedrich A M
Medical College of Virginia, Virginia Commonwealth University, and Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond 23249, USA.
Circulation. 1997 Oct 21;96(8):2509-13. doi: 10.1161/01.cir.96.8.2509.
Autonomic and particularly sympathetic mechanisms play a central role in the pathophysiology of vasovagal syncope. We report direct measurements of muscle sympathetic nerve activity in patients with orthostatic vasovagal syncope.
We studied 53 otherwise healthy patients with orthostatic syncope. We measured RR intervals and finger arterial pressures and in 15 patients, peroneal nerve muscle sympathetic activity before and during passive 60 degree head-up tilt, with low-dose intravenous isoproterenol if presyncope did not develop by 15 minutes. We measured baroreflex gain before tilt with regression of RR intervals or sympathetic bursts on systolic or diastolic pressures after sequential injections of nitroprusside and phenylephrine. Orthostatic vasovagal reactions occurred in 21 patients, including 7 microneurography patients. Presyncopal and nonsyncopal patients had similar baseline RR intervals, arterial pressure, and muscle sympathetic nerve activity. Vagal baroreflex responses were significantly impaired at arterial pressures below (but not above) baseline levels in presyncopal patients. Initial responses to tilt were comparable; however, during the final 200 seconds of tilt, presyncopal patients had lower RR intervals and diastolic pressures than nonsyncopal patients and gradual reduction of arterial pressure and sympathetic activity. Frank presyncope began abruptly with precipitous reduction of arterial pressure, disappearance of muscle sympathetic nerve activity, and RR interval lengthening.
Patients with orthostatic vasovagal reactions have impaired vagal baroreflex responses to arterial pressure changes below resting levels but normal initial responses to upright tilt. Subtle vasovagal physiology begins before overt presyncope. The final trigger of human orthostatic vasovagal reactions appears to be the abrupt disappearance of muscle sympathetic nerve activity.
自主神经尤其是交感神经机制在血管迷走性晕厥的病理生理学中起核心作用。我们报告了对体位性血管迷走性晕厥患者肌肉交感神经活动的直接测量结果。
我们研究了53名其他方面健康的体位性晕厥患者。我们测量了RR间期和手指动脉压，在15名患者中，在被动60度头高位倾斜前及倾斜过程中测量了腓总神经肌肉交感神经活动，若15分钟内未出现前驱晕厥，则静脉注射小剂量异丙肾上腺素。我们在倾斜前通过依次注射硝普钠和去氧肾上腺素后，用RR间期或交感神经爆发对收缩压或舒张压的回归来测量压力反射增益。21名患者出现体位性血管迷走反应，包括7名接受微神经图检查的患者。前驱晕厥患者和未出现前驱晕厥的患者在基线RR间期、动脉压和肌肉交感神经活动方面相似。在前驱晕厥患者中，动脉压低于（但不高于）基线水平时，迷走神经压力反射反应明显受损。对倾斜的初始反应相当；然而，在倾斜的最后200秒内，前驱晕厥患者的RR间期和舒张压低于未出现前驱晕厥的患者，且动脉压和交感神经活动逐渐降低。明显的前驱晕厥突然开始，动脉压急剧下降，肌肉交感神经活动消失，RR间期延长。
体位性血管迷走反应患者对低于静息水平的动脉压变化的迷走神经压力反射反应受损，但对直立倾斜的初始反应正常。在明显的前驱晕厥之前，细微的血管迷走生理变化就已开始。人类体位性血管迷走反应的最终触发因素似乎是肌肉交感神经活动的突然消失。
