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1. How is vasodilation associated with vasovagal syncope?
2. Is nitric oxide involved in the vasovagal syncope?
3. Are there any new initiatives into the triggers of vasovagal syncope?

1. 迷走性晕厥与血管扩张有什么关系？
2. 氧化亚氮与迷走性晕厥是否有关？
3. 是否有新的迷走性晕厥的作用机制？

参考答案：

1.迷走性晕厥与血管扩张有什么关系？

现在认为，导致迷走性晕厥的最终原因为复杂的血管扩张，这也成为很多研究的重点。常认为自主神经张力的变化与血管舒张反射有关，但是这些变化是否促使或伴随迷走性晕厥的出现尚不清楚。虽然早期研究表明，血管扩张诱发迷走性晕厥，但是最近更多研究表明迷走性晕厥出现在血管扩张之前[1]。越来越多的研究者认为，最初人们过大的估计了交感神经的作用，而事实应该是副交感神经系统被激活，交感神经功能减退[2]。需要进行更多的研究以确证和再现直立倾斜试验的诊断价值。

2.氧化亚氮与迷走性晕厥是否有关？

每年的科学分子学研究关注于感兴趣的各个领域，因此对于迷走性晕厥进行相关的研究并不意外。骨骼肌中存在nitroxidergic神经（依靠氧化亚氮的师法而发挥作用的神经），以及在倾斜试验中出现晕厥的患者中发现有氧化亚氮代谢增加的情况下[4]，氧化亚氮的作用尚不清楚。比如，注射氧化亚氮阻滞剂并不能阻止晕厥时的血管扩张[5]。需要更进一步的研究以确证氧化亚氮在迷走性晕厥中的作用。

3.是否有新的迷走性晕厥的作用机制？

近期有研究试图推翻以前的观点，即静脉回流和心室容量减少（Bezold Jarisch反射的结果）是迷走性晕厥的原因。Shen等[6]研究表示，可通过异丙肾上腺素-介导的心脏运动张力的增加和后负荷的减少而诱发迷走性晕厥，并不伴有前负荷的明显减少。最近也有研究试图发现导致迷走性晕厥的其他机制。

How is vasodilation associated with vasovagal syncope?

Profound vasodilation has been considered the final common pathway leading to vasovagal syncope, and as such, is the focus of many investigations. While alterations in autonomic tone are generally accepted to be important to the vasodilatory response, it remains unclear whether these changes promote or follow the vasovagal response. Although earlier work noted that vasodilation promoted the onset of syncope, more recent work has suggested that syncope occurs prior to vasodilation (1). Most investigators rectify this information by suggesting that it represents an initial exaggerated sympathetic output followed by parasympathetic activation and then sympathetic withdrawal (2). Further evidence will be necessary to corroborate and reproduce these effects with diagnostic head-up tilt table testing.

Is nitric oxide involved in the vasovagal syncope?

Science's former molecule of the year appears to be involved with all things interesting, and its involvement in the role of vasovagal syncope is no exception. While the presence of nitroxidergic nerves in skeletal muscle (3) and increased nitric oxide metabolism in patients experiencing syncope on tilt table testing has been observed (4), the role of nitric oxide is not definitive. Infusion of a nitric oxide blocker, for instance, did not prevent vasodilation during syncope (5). Further investigations will need to the extent of nitric oxide's role in vasovagal syncope.

Are there any new initiatives into the triggers of vasovagal syncope?

Many recent investigations have attempted to move away from the idea that decreased venous return and ventricular volume (with the resulting Bezold Jarisch reflex) are responsible for vasovagal syncope. Shen et al. noted that vasovagal syncope could be induced with an isoproterenol-mediated increase in cardiomotor tone and a decrease in afterload, with no significant decreases in preload. Additional mechanisms and triggers are currently being investigated.

Question Author: Lawrence Tsen, MD, Department of Anesthesiology, Perioperative and Pain Medicine, Brigham and Women's Hospital, Harvard Medical School

References:

1. Wallin BG, Sundlof G. Sympathetic outflow to muscles during vasovagal syncope. J Auton Nerv Syst 1982;6(3):287-91.
2. White CM, Tsikouris JP. A review of pathophysiology and therapy of patients with vasovagal syncope. Pharmacotherapy 2000;20(2):158-65.
3. Dietz NM, Halliwill JR, Joyner MJ. Nitric oxide contributes to the rise in forearm blood flow during mental stress in humans. Am J Cardiol. 1998;81:808.
4. Kaufmann H. Neurally mediated syncope: pathogenesis, diagnosis, and treatment. Neurology. 1995;45(4 Suppl 5):S12-8.
5. Dietz NM, Halliwill JR, Spielmann JM, et al. Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans. J Appl Physiol. 1997;82:1785-93.
6. Shen WK, Fenton AM, Lohse CM, et al. Hemodynamic analysis during isoproterenol-induced vasovagal syncope. Am J Cardiol 1997;80:817-22.


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