Aspirin thromboxane A2 and prostacyclin the effect of 100mg aspirin daily on plasma thromboxane A2 and prostacyclin levels

ABSTRACT

In the pathologic events associated with active coronary disease, alterations in the metabolisms of thromboxane A2 [TxA2] and prostacyclin [PGI2] are seen. These may result in disintegration of platelet and vascular wall reactivities accompanying coronary spasm or intravascular thrombosis, associated with myocardial cell necrosis. The main factor relevant with the above mechanisms is the decrease of TxA2/PGI2 ratio. Generally the aim in the treatment concerning these prostanoids is to establish the dose of the drug which inhibits TxA2 maximally and PGI2 minimally. This study has been performed with this aim in 10 healthy volunteers, age varying between 17 and 48. 100 mg/day aspirin's single dose and the15 days long usage of the same amount's effect have been investigated on plasma TxA2and PGI levels. Plasma values of TxB2 and 6 - keto PGF1alpha [stable metabolites of TxA2 and PGI2, respectively] have been measured with the tritium labeled radioimmunassay kits of Nen Firm [Cat. No. NEK 007 and 008, respectively]. 100 mg/day aspirin's single dose have caused inhibition on TxB2 and 6 - keto PGF2 alpha respectively as 82.3% and 58.3%. After long term usage these inhibitions were again respectively 96.8% and 85.1%. A a result, it has been found out that, after long term usage of 100 mg aspiring daily, TxB2 30.75, while 6 - keto PGF1 alpha 6.70 times were decreased compared to the control groups' mean values