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Long-lived inhibition of anodal current-induced vasodilation by oral single high dose aspirin



Long-lived inhibition of anodal current-induced vasodilation by oral single high dose aspirin



FASEB Journal 17(4-5): Abstract No 77 8



Previously we reported that acetyl salicyclic acid (aspirin) inhibits anodal current-induced cutaneous vasodilation (AnVAS). Aspirin irreversibly blocks cyclooxygenase (COX), which is necessary for prostaglandin (PG) synthesis. Recovery of COX is faster in endothelial or smooth muscle cells (3 to 36 hours) than in platelets (up to 10 days). By assessing the time course of aspirin inhibition of AnVAS, the origin of PG involved in this response may be identified. Forearm AnVAS was recorded following 20 minutes of 5 min, 0.10mA transcutaneous anodal current application, using deionised water as a vehicle. Peak AnVAS was normalised relative to maximal cutaneous vasodilation (44(C local heating). Experiments were performed before and 2 hours, 10 hours, 3 days, 7 days, 10 days, and 14 days after blinded administration of 1-g aspirin or placebo.Peak AnVAS (mean(SD; aspirin vs placebo) was 13.6(14.5 vs. 65.0(32.1 (2 hours; p< 0.05), 14.7(4.2 vs. 87.5(31.9 (10 hours; p< 0.05), 18.1(10.2 vs. 71.6(26.8 (3 days; p< 0.05), 42.5(23.4 vs. 73.3(26.8 (7 days; non significant, NS), 60.2(24.3 vs. 75.2(26.9 (10 days; NS), 52.1(18.5 vs. 67.9(32.1 (14 days; NS). Inhibition of AnVAS persisted long after endothelial and smooth muscle COX are restored. Thus, PG involved in AnVAS are not endothelial-or smooth muscle-derived. The mechanism of prolonged inhibition of AnVAS by aspirin remains to be identified.

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