Dietz N M, Joyner M J, Shepherd J T
Mayo Foundation, Rochester, Minnesota, USA.
Pacing Clin Electrophysiol. 1997 Mar;20(3 Pt 2):775-80. doi: 10.1111/j.1540-8159.1997.tb03903.x.
During vasovagal syncope, profound bradycardia and hypotension occur. Atropine administration can prevent the bradycardia but not the hypotension, suggesting that marked peripheral vasodilation is a major cause of the fall in arterial pressure. This concept has been confirmed since vasovagal syncope can be seen in patients who have undergone heart transplantation and also in patients subject to cardiac pacing. In both cases, there is no bradycardia but hypotension during the syncopal attacks. The major site of the vasodilation is in skeletal muscle and muscle sympathetic nerve activity is suppressed just prior to and during vasovagal attacks, indicating that sympathetic withdrawal contributes to the dilation. However, the skeletal muscle vasodilation seen during syncope is greater than that caused by sympathetic withdrawal alone, and it is absent in limbs that have undergone surgical sympathectomy, or local anesthetic nerve block. These observations suggest a role for neurally mediated "active" vasodilation during syncope. The afferent neural pathways that evoke the profound vasodilation during vasovagal attacks remain the subject of debate. The neural pathways responsible for the active component of the dilation are also unknown. Recent evidence has demonstrated that cholinergic, beta-adrenergic, and nitroxidergic (nitric oxide) vasodilator mechanisms are not essential to observe the dilation, demonstrating that the mechanisms responsible for it remain a continuing conundrum.
在血管迷走性晕厥期间，会出现严重的心动过缓和低血压。给予阿托品可预防心动过缓，但不能预防低血压，这表明明显的外周血管舒张是动脉压下降的主要原因。这一概念已得到证实，因为在心脏移植患者以及接受心脏起搏的患者中都可出现血管迷走性晕厥。在这两种情况下，晕厥发作期间均无心动过缓，但有低血压。血管舒张的主要部位在骨骼肌，并且在血管迷走性发作之前及发作期间肌肉交感神经活动受到抑制，这表明交感神经活动减弱促成了血管舒张。然而，晕厥期间所见的骨骼肌血管舒张大于仅由交感神经活动减弱所引起的血管舒张，并且在接受手术交感神经切除术或局部麻醉神经阻滞的肢体中不存在这种情况。这些观察结果提示在晕厥期间神经介导的“主动”血管舒张起了作用。引发血管迷走性发作期间深度血管舒张的传入神经通路仍是争论的焦点。负责血管舒张主动成分的神经通路也尚不清楚。最近的证据表明，胆碱能、β-肾上腺素能和一氧化氮能血管舒张机制对于观察到血管舒张并非必不可少，这表明其背后的机制仍然是一个未解之谜。
