Effect of triflusal on the platelet aggregation in human whole blood.
- Author:
Hye Seung LEE
1
;
Kyung Soo KANG
;
Byung Chul LEE
;
Kyung Ho YU
Author Information
1. Department of Neurology Hallym University College of Medicine.
- Publication Type:In Vitro ; Original Article ; Randomized Controlled Trial
- MeSH:
Adenosine Diphosphate;
Adenosine Triphosphate;
Aspirin;
Blood Platelets*;
Collagen;
Eating;
Electric Impedance;
Healthy Volunteers;
Humans*;
Male;
Platelet Aggregation*;
Prostaglandin-Endoperoxide Synthases;
Thromboxane B2
- From:Journal of the Korean Neurological Association
1997;15(1):60-66
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND AND PURPOSE: Triflusal(TR), 2-acetoxy-4-trifluoromethyl banzoic acid, is a platelet aggregation inhibitor structurally related to aspirin, proven to possess both in vitro and in vivo platelet antiaggregatoy activity. The aim of this study was to evaluate the effect of TR with different dosages on platelet function using platelet aggregation, adenosine triphosphate (ATP) secretion, and thromboxane generation after TR administration. METHODS: Twenty healthy volunteers (age 25-41years, 15 males 5 females) were randomly divided into two groups of ten subjects who were receiving one of two regimens (TR 300mg/day; TR 900mg/day) for seven days. Platelet functions including platelet aggregation by impedance methods using whole blood with ADP (5, 10uM) and collagen (1,2uM), ATP secretion and thromboxane B2 generation were determined. RESULTS: The inhibitory effect of platelet aggregation was observed in both groups. The degree of inhibitory effect was depended on the dosage of TR and the types of aggregating agent. Thromboxane B2 concentrations were significantly decreased by TR ingestion in both groups (p<0.01), but there was no differences in ATP secretion. CONCLUSIONS: This study show that TR exerts a remarkable platelet antiaggregation effect and inhibition of thromboxane synthesis in whole blood. In addition, the fact that TR does not affect ATP secretion means selective blocking of the platelet cyclooxygenase pathway.
