Thromb Haemost 2004; 91(01): 119-128
DOI: 10.1160/TH03-05-0330
Platelets and Blood Cells
Schattauer GmbH

The influence of selective serotonin reuptake inhibitors on human platelet serotonin

Elisabeth Maurer-Spurej
1   Canadian Blood Services, Vancouver, British Columbia, Canada
2   University of British Columbia, Department of Pathology, Vancouver, British Columbia, Canada
,
Cheryl Pittendreigh
1   Canadian Blood Services, Vancouver, British Columbia, Canada
,
Kevin Solomons
3   Department of Psychiatry, Vancouver, British Columbia, Canada
› Author Affiliations
Further Information

Publication History

Received 30 May 2003

Accepted after resubmission 25 September 2003

Publication Date:
30 November 2017 (online)

Summary

Clinical depression has been proposed to be an independent risk factor for cardiovascular disease. While it is suggested that selective serotonin reuptake inhibitors (SSRIs) reduce the risk of acute cardiovascular problems of depressed patients, the effect of SSRIs on platelets, the only blood cells committed to serotonin (5-HT) transport, remains largely unknown. The goal of this pilot study was to measure the 5-HT levels in platelets of untreated and SSRI-treated depressed patients and normal subjects and to determine whether the interaction of SSRIs with platelets can explain their possible cardiovascular benefit in patients with depression. Platelet 5-HT was determined by an immunocytochemical assay and high-pressure liquid chromatography with electrochemical detection (HPLC-ECD). In normal control subjects without cardiovascular disease, 78 ± 8% of platelets were 5-HT-positive (n = 14). Depression caused a significant reduction in platelet 5-HT to 46 ± 21% in untreated patients (n = 13) and 22 ± 13% in SSRI-treated patients (n = 14). As a class, all selective serotonin reuptake inhibitors significantly reduced the 5-HT concentration in patient platelets. An inverse relationship of 5-HT level and dose of medication might be suggested. These results correlated well with 5-HT data from HPLC (r = 0.8509, p < 0.001). SSRIs did not affect platelet aggregation and dense granule release in response to thrombin, but significantly reduced ADP-induced platelet aggregation and dense granule release in both patient and normal control samples. The active inhibition of platelet aggregation by SSRIs might explain their cardiovascular benefit.

 
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