Abstract
Introduction: Early detection of endothelial dysfunction, characterized by a reduced bioavailability of NO, is essential as it is a key phenomenon in the genesis of cardiovascular diseases. Heat-induced vasodilatation is mediated mainly by NO, as shown by L Name (L) microdialysis. L Name is a competitive inhibitor of cNOS, produced by the vascular endothelium, and is polarized negatively. The application of a microcurrent on the skin allows polarized molecules, such as sodium nitroprusside and acetylcholine, to penetrate into the dermis. Whether L Name iontophoresis is feasible, and will reduce skin blood flow measured by a laser Doppler imager (LDI) in response to heating, is not known. We also assessed whether this response is dose-dependent. Last, we compared this response between habitual smokers and non smokers. Methods: In a population of 17 healthy male smokers and 17 matched healthy male non-smokers (aged 28 years ± 5 yrs, BMI 22 ± 3 kg/m2), we conducted an iontophoresis of L Name and placebo on the two arms on Day 0. This was repeated with the same dose, and a double dose of L, on Day 4, on both arms. After iontophoresis, the sites were heated to 44°C to induce vasodilation, and scanned to measure blood flow in the microcirculation. We also determined pulse wave velocity in both groups. Smoking was forbidden 12 hours before the experiments. Results: L Name decreased equally blood flow during heating in the non smokers and smokers (p < 0.01, table 1). Both concentrations of 20 and 40 mM of L Name were equally effective. Pulse wave velocity was normal at 9 m/s, and did not differ between groups.Conclusion: L Name iontophoresis is feasible and is able to inhibit vascular endothelial NOS. Higher concentrations of L Name than 20 mM do not provide further vasodilatation. NO-mediated skin blood flow vasodilatation is not altered in healthy young sportive smokers investigated after 12 hours of smoking cessation.
Published Version
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