Aims The hypotensive reflex responsible for vasovagal syncope appears relat
ed to a reduction in sympathetic neural outflow. Several animal studies sug
gest that serotonin may play a role in the genesis of this reflex, through
inhibition of sympathetic activity. However, the role of the serotonergic s
ystem 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 mea
ns of the level of platelet and plasma serotonin, as well as plasma catecho
lamines. during tilt-induced syncope.
Methods and Results Fifteen patients (age 34 +/- 16 years) with vasovagal s
yncope underwent a head-up tilt test (HUT, 60 degrees, 45 min). If syncope
did not develop, 300 mug nitroglycerin was administered sublingually and pa
tients continued to be tilted for a further 20 min. Blood samples were obta
ined in the supine position, and then after 3, 10, 15, 30, 45, 48 and 65 mi
n of HUT. If syncope developed, blood samples were obtained at the beginnin
g 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 pa
tients developed syncope during the unmedicated HUT and four after nitrogly
cerin. In these patients plasma adrenaline significantly increased from the
last programmed sample before the prodrome to its beginning and showed a f
urther increase during loss of consciousness, whereas plasma noradrenaline
did not increase, as an expression of inhibition of sympathetic neural outf
low. In the patients experiencing syncope, both platelet and plasma seroton
in showed no significant change after tilt-up, at the beginning of prodrome
, during syncope and after recovery of consciousness.
Conclusion These results do not suggest that the serotonergic system plays
a role in the pathophysiology of vasovagal syncope. (Europace 2000: 2: 172-
180) (C) 2000 The European Society of Cardiology.