Intended for healthcare professionals

Research Article

Sulphinpyrazone and the platelet serotoninergic mechanism in ischaemic heart disease.

Br Med J (Clin Res Ed) 1986; 293 doi: (Published 06 September 1986) Cite this as: Br Med J (Clin Res Ed) 1986;293:591
  1. V K Puri,
  2. A Rawat,
  3. A Sharma,
  4. A Mehrotra,
  5. M Hasan,
  6. K Shanker,
  7. M Verma,
  8. J N Sinha,
  9. K P Bhargava


    A double blind study in 25 patients with ischaemic heart disease and 20 matched healthy controls examined the effect of sulphinpyrazone on the uptake of serotonin by platelets and the basal concentrations of serotonin in platelets. Uptake was measured using tritium labelled serotonin and basal concentrations estimated spectrophotofluorometrically. Serotonin uptake was significantly increased both in the patients with chronic stable angina of effort and in those with a history of myocardial infarction six months or more previously. Sulphinpyrazone reduced serotonin uptake from 94.25 (SE 8.65) to 57.86 (5.37) cpm/10(8) platelets after 24 weeks of treatment in the group with stable angina and from 137.45 (16.26) to 68.08 (8.38) cpm/10(8) platelets in the myocardial infarction group. Raised basal concentrations in the two groups were also reduced by sulphinpyrazone. Placebo had no effect on serotonin uptake or basal concentrations in either group of patients. The ability of sulphinpyrazone to inhibit uptake and reduce basal concentrations of serotonin in patients with ischaemic heart disease may be yet another mechanism through which this drug exerts its beneficial antiplatelet effect.