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.
Possible Hypoxia Signaling Induced Alteration of Glucose Homeostasis in Rats Exposed to Chronic Intermittent Hypoxia - Role of Antioxidant (Vitamin C) and Ca2+ Channel Blocker (Cilnidipine)
