Mosqueda-Garcia R, Furlan R, Fernandez-Violante R, Desai T, Snell M, Jarai Z, Ananthram V, Robertson R M, Robertson D
Syncope Service in the Autonomic Dysfunction Unit, Vanderbilt University Medical Center, Nashville, Tennessee 37232-2195, USA.
J Clin Invest. 1997 Jun 1;99(11):2736-44. doi: 10.1172/JCI119463.
The pathophysiology of neurally mediated syncope is poorly understood. It has been widely assumed that excessive sympathetic activation in a setting of left ventricular hypovolemia stimulates ventricular afferents that trigger hypotension and bradycardia. We tested this hypothesis by determining if excessive sympathetic activation precedes development of neurally mediated syncope, and if this correlates with alterations in baroreflex function. We studied the changes in intraarterial blood pressure (BP), heart rate (HR), central venous pressure (CVP), muscle sympathetic nerve activity (MSNA), and plasma catecholamines evoked by upright tilt in recurrent neurally mediated syncope patients (SYN, 5+/-1 episodes/mo, n = 14), age- and sex-matched controls (CON, n = 23), and in healthy subjects who consistently experienced syncope during tilt (FS+, n = 20). Baroreflex responses were evaluated from changes in HR, BP, and MSNA that were obtained after infusions of phenylephrine and sodium nitroprusside. Compared to CON, patients with SYN had blunted increases in MSNA at low tilt levels, followed by a progressive decrease and ultimately complete disappearance of MSNA with syncope. SYN patients also had attenuation of norepinephrine increases and lower baroreflex slope sensitivity, both during tilt and after pharmacologic testing. FS+ subjects had the largest decrease in CVP with tilt and had significant increases in MSNA and heart rate baroreflex slopes. These data challenge the view that excessive generalized sympathetic activation is the precursor of the hemodynamic abnormality underlying recurrent neurally mediated syncope.
神经介导性晕厥的病理生理学机制尚不清楚。人们普遍认为，在左心室血容量不足的情况下，过度的交感神经激活会刺激心室传入神经，进而引发低血压和心动过缓。我们通过确定过度的交感神经激活是否先于神经介导性晕厥的发生，以及这是否与压力反射功能的改变相关，来验证这一假设。我们研究了复发性神经介导性晕厥患者（SYN，每月发作5±1次，n = 14）、年龄和性别匹配的对照组（CON，n = 23）以及在倾斜试验中始终出现晕厥的健康受试者（FS +，n = 20）在直立倾斜过程中动脉内血压（BP）、心率（HR）、中心静脉压（CVP）、肌肉交感神经活动（MSNA）和血浆儿茶酚胺的变化。通过注射去氧肾上腺素和硝普钠后获得的HR、BP和MSNA的变化来评估压力反射反应。与CON相比，SYN患者在低倾斜水平时MSNA的增加减弱，随后逐渐减少，最终在晕厥时MSNA完全消失。SYN患者在倾斜过程中和药物测试后，去甲肾上腺素增加的幅度也减弱，压力反射斜率敏感性降低。FS +受试者在倾斜时CVP下降幅度最大，MSNA和心率压力反射斜率显著增加。这些数据对过度的全身性交感神经激活是复发性神经介导性晕厥潜在血流动力学异常的先兆这一观点提出了挑战。
