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2 results on '"Lauciello C"'

1. Effect of picotamide on platelet aggregation and on thromboxane A2 production in vivo.

Author

Minuz P, Lechi C, Arosio E, Guzzo P, Zannoni M, Lauciello C, and Lechi A

Subjects
Aged, Arteriosclerosis Obliterans blood, Arteriosclerosis Obliterans urine, Epoprostenol urine, Humans, Male, Middle Aged, Thromboxane A2 blood, Thromboxane A2 urine, Phthalic Acids pharmacology, Platelet Aggregation Inhibitors, Thromboxane A2 biosynthesis
Abstract

Effects of picotamide (900 mg in 3 oral administrations for 7 days) on ex vivo and in vivo platelet TxA2 production and on platelet aggregation were 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 TxA2 production (TxB2 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-TXB2 (in vivo indicator of platelet TxA2 production), or on in vivo PGI2 production (urinary excretion of 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha). In the same subjects, single-dose aspirin reduced ex vivo TxB2 production by at least 98% and 2,3-dinor-TxB2 excretion from 116.7 +/- 61.4 to 32.6 +/- 17.0 ng/g 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 TxA2 production in vivo may not be picotamide's main mechanism of action.

Published
1991

2. Effect of picotamide on platelet aggregation and on thromboxane A2 production in vivo

Author

Minuz, Pietro, Lechi, C., Arosio, Enrico, Guzzo, P., Paluani, F., Zannoni, M., Lauciello, C., and Lechi, A.

Subjects
Male, medicine.medical_specialty, picotamide, thromboxane, platelet aggregation, Thromboxane, Phthalic Acids, thromboxane A2, Excretion, chemistry.chemical_compound, Thromboxane A2, In vivo, Internal medicine, medicine, Picotamide, Humans, Platelet, Aged, platelet, Creatinine, Chemistry, aggregation, Hematology, Arteriosclerosis Obliterans, Middle Aged, Epoprostenol, Endocrinology, Immunology, Ex vivo, Platelet Aggregation Inhibitors, medicine.drug
Abstract

SummaryEffects 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-PGF1α and 2,3-dinor-6-keto-PGF1α). 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.

Published
1991

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