Skin blood flow response to topically applied methyl nicotinate: Possible mechanisms.

Abstract

Methyl nicotinate (MN) induces a local cutaneous erythema in the skin and may be valuable as a local provocation in the assessment of microcirculation and skin viability. The mechanisms through which MN mediates its vascular effect are not fully known. The aim of this study was to characterize the vasodilatory effects of topically applied MN and to study the involvement of nitric oxide (NO), local sensory nerves, and prostaglandin-mediated pathways. MN was applied on the skin of healthy subjects in which NO-mediated (L-NMMA), nerve-mediated (lidocaine/prilocaine), and cyclooxygenase-mediated (NSAID) pathways were selectively inhibited. Microvascular responses in the skin were measured using laser speckle contrast imaging (LSCI). NSAID reduced the MN-induced perfusion increase with 82% (P<.01), whereas lidocaine/prilocaine reduced it with 32% (P<.01). L-NMMA did not affect the microvascular response to MN. The prostaglandin pathway and local sensory nerves are involved in the vasodilatory actions of MN in the skin.