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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 β‐thromboglobulin (β‐TG)). Results. During hyperoxaemia in humans, serum concentrations of serotonin and β‐TG remained unchanged. Conclusion: 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.