shown the levels of f-5HT in plasma are increased in symptomatic patients
with asthma. In addition, the concentration of f-5HT in symptomatic
asthmatic patients correlates positively with clinical status and negatively
with pulmonary function (FEV1) (Figure).
Tianeptine provoked a dramatic and sudden decrease of both clinical
rating and f-5HT plasma levels and an increase in pulmonary function
(References: Lechin et al., Ann Allergy Asthma & Immunol 1996, 77:245-253;
Lechin et al., Clin Pharmacol Ther 1998,64:223-232; Lechin et al., J
Clin Pharmacol 1998, 38:918-925).
Although adrenal catecholamines (adrenaline and noradrenaline) were found
to be raised in symptomatic asthmatic patients, no correlations were
found between these neurotransmitters when plotted against clinical
rating and pulmonary function (FEV1). However, raised levels of plasma
adrenaline are able to trigger platelet aggregation which in turn are
responsible for the increase of plasma f-5HT. The pathophysiologic mechanisms
involved in the etiopathogenic role displayed by f-5HT on asthma attacks
include the release of acetylcholine by parasympathetic nerves as well
as mast cell degranulation. Serotonin released at central medullary
level provokes exciting of both respiratory and vagal nuclei.
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