Effect of Picotamide on Platelet Aggregation and on Thromboxane A2 Production In Vivo

P Minuz; C Lechi; E Arosio; P Guzzo; M Zannoni; C Lauciello; A Lechi

doi:10.1055/s-0038-1648141

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 1991; 65(03): 312-316
DOI: 10.1055/s-0038-1648141

Original Article

Schattauer GmbH Stuttgart

Effect of Picotamide on Platelet Aggregation and on Thromboxane A₂ Production In Vivo

P Minuz

¹The Istituti di Clinica Medica, University of Verona, Verona, Italy

,

C Lechi

²The e Chimica Clinica, University of Verona, Verona, Italy

,

E Arosio

¹The Istituti di Clinica Medica, University of Verona, Verona, Italy

,

P Guzzo

²The e Chimica Clinica, University of Verona, Verona, Italy

,

M Zannoni

¹The Istituti di Clinica Medica, University of Verona, Verona, Italy

,

C Lauciello

²The e Chimica Clinica, University of Verona, Verona, Italy

,

A Lechi

¹The Istituti di Clinica Medica, University of Verona, Verona, Italy

› Author Affiliations

Abstract

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Summary

Effects of picotamide (900 mg in 3 oral administrations for 7 days) on ex vivo and in vivo platelet T×A₂ production and on platelet aggregation wpre evaluated in 8 patients with peripheral arteriopathy and in 8 normal subjects. Picotamide significantly reduced ADP-induced platelet aggregation, but had no effect on that induced by arachidonic acid or the thromboxane analogue U46619. Though ex vivo platelet T×A₂ production (T×B₂ concentration after arachidonic-acid-induced aggregation) was reduced from 946 ± 141 (mean ± SD) to 285 ± 91 ng/ml in controls and from 1515 ± 673 to 732 ± 420 ng/ml in patients with arteriopathy, there was no effect on urinary excretion of 2,3-dinor-T×B₂ (in vivo indicator of platelet T×A₂ production), or on in vivo PGI₂ production (urinary excretion of 6-keto-PGF_1α and 2,3-dinor-6-keto-PGF_1α). In the same subjects, single-dose aspirin reduced ex vivo T×B₂ production by at least 98% and 2,3-dinor-T×B₂ excretion from 116.7 ± 61.4 to 32.6 ± 17.0 nglg creatinine in control subjects, and from 156.3 ± 66.1 to 59.1 ± 19.2 ng/g creatinine in patients with peripheral arteriopathy. Our data suggest that inhibition of platelet T×A₂ production in vivo may not be picotamide’s main mechanism of action.

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References

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