Alboni P, Bondanelli M, Dinelli M, Gruppillo P, Franceschetti P, Marchi P, degli Uberti E C
Division of Cardiology, Ospedale Civile, Cento, Fe, Italy.
Europace. 2000 Apr;2(2):172-80. doi: 10.1053/eupc.1999.0088.
The hypotensive reflex responsible for vasovagal syncope appears related to a reduction in sympathetic neural outflow. Several animal studies suggest that serotonin may play a role in the genesis of this reflex, through inhibition of sympathetic activity. However, the role of the serotonergic system is unknown in humans. The purpose of the study was to investigate the role of the serotonergic system in the genesis of vasovagal syncope by means of the level of platelet and plasma serotonin, as well as plasma catecholamines, during tilt-induced syncope.
Fifteen patients (age 34 +/- 16 years) with vasovagal syncope underwent a head-up tilt test (HUT, 60 degrees , 45 min). If syncope did not develop, 300 microg nitroglycerin was administered sublingually and patients continued to be tilted for a further 20 min. Blood samples were obtained in the supine position, and then after 3, 10, 15, 30, 45, 48 and 65 min of HUT. If syncope developed, blood samples were obtained at the beginning of the prodrome, during syncope and after the recovery of consciousness. Platelet and plasma serotonin and plasma catecholamines were measured using high-pressure liquid chromatography with electrochemical detection. Ten patients developed syncope during the unmedicated HUT and four after nitroglycerin. In these patients plasma adrenaline significantly increased from the last programmed sample before the prodrome to its beginning and showed a further increase during loss of consciousness, whereas plasma noradrenaline did not increase, as an expression of inhibition of sympathetic neural outflow. In the patients experiencing syncope, both platelet and plasma serotonin showed no significant change after tilt-up, at the beginning of prodrome, during syncope and after recovery of consciousness.
These results do not suggest that the serotonergic system plays a role in the pathophysiology of vasovagal syncope.
负责血管迷走性晕厥的降压反射似乎与交感神经传出减少有关。多项动物研究表明，血清素可能通过抑制交感神经活动在该反射的发生中起作用。然而，血清素能系统在人类中的作用尚不清楚。本研究的目的是通过倾斜诱发晕厥期间血小板和血浆血清素水平以及血浆儿茶酚胺来研究血清素能系统在血管迷走性晕厥发生中的作用。
15例血管迷走性晕厥患者（年龄34±16岁）接受了头高位倾斜试验（HUT，60度，45分钟）。如果未发生晕厥，则舌下含服300微克硝酸甘油，患者继续倾斜20分钟。在仰卧位以及HUT 3、10、15、30、45、48和65分钟后采集血样。如果发生晕厥，则在先兆期开始时、晕厥期间和意识恢复后采集血样。使用带有电化学检测的高压液相色谱法测量血小板和血浆血清素以及血浆儿茶酚胺。10例患者在未用药的HUT期间发生晕厥，4例在使用硝酸甘油后发生晕厥。在这些患者中，血浆肾上腺素从先兆期前的最后一个设定样本到其开始时显著增加，并在意识丧失期间进一步增加，而血浆去甲肾上腺素没有增加，这是交感神经传出抑制的表现。在发生晕厥的患者中，倾斜后、先兆期开始时、晕厥期间和意识恢复后，血小板和血浆血清素均无显著变化。
这些结果并不表明血清素能系统在血管迷走性晕厥的病理生理学中起作用。
