THE ROLE OF SEROTONIN AS A MEDIATOR OF EMESIS INDUCED BY DIFFERENT STIMULI

The aim of this work was to evaluate the impact of changes in serotoni n metabolism on the pathophysiology of different types of emesis: preg nancy-induced emesis, emesis associated with inner-ear dysfunction, an d cisplatin-induced emesis. The urinary excretion of 5-hydroxyindoleac etic acid (5-HIAA), the main metabolite of serotonin, was measured in 13 women with pregnancy-induced emesis, 12 patients who had nausea and vomiting following inner-ear dysfunctions, 27 patients with cisplatin -induced emesis and a control group of 21 women. 5-HIAA was measured w ith a fluorescence polarization immunoassay (Abbott) and corrected for varying urine concentrations. Both patients with emesis associated wi th inner-ear dysfunction and patients with pregnancy-associated emesis showed a similar 5-HIAA excretion pattern compared with the control g roup. No correlation between intensity of nausea or vomiting and chang es in 5-HIAA excretion could be detected. Tn patients receiving cispla tin, the 5-HIAA excretion increased rapidly within the 12 h following cisplatin administration and returned to baseline levels after 24 h. T here was a parallel increase of 5-HIAA excretion and numbers of emetic episodes in the first 12 h, but delayed emesis was not associated wit h elevated 5-HIAA excretion. Our results provide evidence that seroton in is involved in the pathophysiology of cisplatin-induced acute emesi s. Cisplatin-induced delayed emesis, pregnancy-associated emesis, and emesis due to inner-ear dysfunction are not associated with elevated l evels of 5-HIAA excretion. The serotonin pathway probably represents o nly one of many different afferent mechanisms capable of initiating th e emesis cascade.