Hyperoxaemia does not change concentrations of serotonin and beta-thromboglobulin in blood of healthy humans.
BACKGROUND
The mechanisms of oxygen-induced effects on blood vessels (vasoconstriction in hyperoxaemia and vasodilatation during hypoxaemia) are uncertain. Many investigators have suggested that the vasoconstriction seen during hyperoxia/hyperoxaemia is mediated through the endothelium as a result of either increased release or activity of vasoconstrictors (oxygen radicals, endothelin, norepinephrine, angiotensin II, or serotonin (5-HT)), or reduced activity of vasodilators (prostaglandin E2 and nitric oxide). Serotonin has been assumed to have a central role.


METHODS
Eight healthy volunteers were exposed to FiO2 of 1.0 for 20 min and serum concentrations of serotonin and activated platelets were measured (indicated by concentrations of beta-thromboglobulin (beta-TG)).


RESULTS
During hyperoxaemia in humans, serum concentrations of scrotonin and beta-TG remained unchanged.


CONCLUSIONS
If serotonin is involved in oxygen-induced vasoconstriction, the mechanism is more likely to be either a potentiating effect of serotonin on other vasoconstrictors or increased activity of serotonin on its receptor.
Rousseau
A
A
Department of Anaesthesiology and Intensive Care and the Burn Intensive Care Unit, Faculty of Health Sciences, University Hospital, Linköping, Sweden.
Abdiu
A
A
Sjöberg
F
F
D000328:Adult; D005260:Female; D006801:Humans; D018496:Hyperoxia / Q000097:blood*; D008297:Male; D012701:Serotonin / Q000097:blood*; D001620:beta-Thromboglobulin / Q000032:analysis*
D001620:beta-Thromboglobulin; D012701:Serotonin