Why the study?
Does sulphinpyrazone reduce thromboxane A2 production in healthy volunteers?
Does sulphinpyrazone reduce thromboxane A2 production in healthy volunteers?
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Sulphinpyrazone reduces proaggregatory TxA2 without affecting antiaggregatory PGI2, shifting the balance toward antiaggregation.
We studied the effect of 3 weeks' treatment with 4 x 200 mg of sulphinpyrazone daily (six healthy volunteers) on proaggregatory thromboxane A2 (TxA2) and antiaggregatory prostacyclin (PGI2). Platelet TxA2 production was evaluated by measuring its stable metabolite, immunoreactive thromboxane B2, from serum, and vessel wall PGI2 production by measuring its stable metabolite, immunoreactive 6-keto-prostaglandin F1 alpha in plasma. The TxA2 production (initially 209.0 +/- 27.1 ng/ml, mean +/- s.e. mean) decreased to about 30% from the second day of the treatment onwards, and it recovered in three days after the discontinuation of the treatment. PGI2 (initially 33.6 +/- 3.6 pg/ml) did not change. The shift of the balance between TxA2 and PGI2 to the dominance of antiaggregatory PGI2 during sulphinpyrazone treatment may be involved with the efficacy of the drug in the secondary prevention of myocardial infarction.
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Viinikka et al. (1982) studied this question.
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