In healthy young men (age, 20–22 years), we tested the role of prostanoids produced by the COX (cyclo-oxygenase) pathway in cutaneous vasodilatation evoked in the finger by ACh (acetylcholine). To this end, changes in cutaneous RCF (red cell flux), recorded by the laser Doppler technique, evoked by a series of iontophoretic pulses of ACh were tested before and after oral aspirin (600 mg). Increases in RCF produced by successive pulses of ACh up to a mean change of 125.5±11.8 PU (perfusion units) were potentiated 30 min after aspirin (160.0±12.4 PU; P<0.05). By contrast, aspirin had no effect on increases in RCF evoked by iontophoretic application of the NO (nitric oxide) donor and endothelium-independent dilator sodium nitroprusside (mean increases in RCF were 73.8±9.8 PU before and 79.1±12.2 PU after aspirin). The ACh-evoked increases in RCF were also potentiated 3 h after oral administration of the antioxidant vitamin C (1000 mg; 139.1±15.4 PU before and 170.5±13.5 PU after vitamin C; P<0.05). We propose that, in healthy young men, cutaneous vasodilatation evoked in the finger by the endothelium-dependent dilator ACh is limited by constrictor products of the COX pathway, including PGH2 (prostaglandin H2), TXA2 (thromboxane A2) and/or superoxide anions. This effect of the COX products may be an early marker of the increased risk of cardiovascular disease in men compared with women.

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