Autonomic control of vasovagal syncope
Autonomic control of vasovagal syncope
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DOI：
10.1152/ajpheart.1998.274.6.h2110
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发表时间：
1998-06-01
影响因子：
4.8
通讯作者：
Crozier, IG
中科院分区：
文献类型：
--
作者：
Jardine, DL;Ikram, H;Crozier, IG
在血管迷走性晕厥的病理生理学研究中，压力感受器敏感性（BS）、交感神经退缩和副交感神经活动之间相互作用的性质尚未确定。改变的BS可能倾向于对直立的异常交感神经和副交感神经反应，引起低血压，如果交感神经退缩，则可能进展为晕厥。为了验证这一假设，我们连续监测了18名血管迷走神经患者在60度头高位倾斜、晕厥和恢复期间的血压（BP）、心率（HR）、BS、前臂血流量和肌肉神经交感活性（MNSA）。结果与17例能耐受倾斜45 min的患者进行比较。在倾斜早期，两组患者的血压均通过HR和MNSA较基线增加而得以维持（P < 0.01），但晕厥组的BS下降幅度更大（P < 0.05）。在晕厥前期开始时（晕厥前平均2.7 ± 0.2 min，倾斜后平均15.2 ± 12 min），当血压下降时，心率和交感神经活性仍较基线增加（P < 0.01）。此后，血压和心率与交感神经活性直接相关，并以线性方式回归，直至晕厥（P < 0.001），而BS则增加至基线。晕厥时，血压、心率和交感神经活性均低于基线水平（分别为P <0.01、P < 0.05和P < 0.01），但BS没有增加。恢复期交感神经活性恢复至基线水平，BS增加（P < 0.05），而HR和BP保持较低水平（分别为P < 0.01和P <0.05）。晕厥前期低血压的发生机制尚不清楚，但BS可能起作用。晕厥前期的血管舒张和心动过缓似乎与交感神经活动的消退比与副交感神经心脏活动的增加更密切相关。
In the pathophysiological study of vasovagal syncope, the nature of the interaction between baroreceptor sensitivity (BS), sympathetic withdrawal, and parasympathetic activity has yet to be ascertained. Altered BS may predispose toward abnormal sympathetic and parasympathetic responses to orthostasis, causing hypotension that may progress to syncope if there is sympathetic withdrawal. To examine this hypothesis, we monitored blood pressure (BP), heart rate (HR), BS, forearm blood flow and muscle nerve sympathetic activity (MNSA) continuously in 18 vasovagal patients during 60 degrees head-up tilt, syncope, and recovery. Results were compared with those of 17 patients who were able to tolerate tilt for 45 min. During early tilt, BP was maintained in both groups by an increase in HR and MNSA from baseline (P < 0.01), but BS decreased more in the syncopal group (P < 0.05). At the start, of presyncope (mean 2.7 +/- 0.2 min before syncope and 15.2 +/- 12 min after tilt), when BP fell, HR and sympathetic activity remained increased from baseline (P < 0.01). Thereafter BP and HR correlated directly with sympathetic activity and regressed in Linear fashion until syncope (P < 0.001), whereas BS increased to baseline. At syncope, BP, HR, and sympathetic activity fell below baseline (P ( 0.01, P < 0.05, and P < 0.01, respectively), but BS did not increase. During recovery, sympathetic activity increased to baseline and BS increased (P < 0.05), whereas HR and BP remained low (P < 0.01 and P ( 0.05, respectively). The mechanism for the initiation of hypotension during presyncope remains unknown, but BS may contribute. Vasodilatation and bradycardia during presyncope appear to be more closely related to withdrawal of sympathetic activity than to increased parasympathetic cardiac activity.