Transient hyperaemic response to assess skin vascular reactivity: effects of heat and iontophoresed norepinephrine.

Abstract

Forearm skin vascular reactivity may be assessed using a transient hyperaemic response (THR) after 20 s of brachial artery compression. THR has been manipulated by iontophoresis of vasodilators, but not vasoconstrictors, possibly because of low baseline blood flow. The effects of vasoconstrictors on vascular reactivity of pre-dilated blood vessels are unknown. We have investigated this using locally applied heat to vasodilate the skin microcirculation before iontophoresis of norepinephrine. Active and control laser Doppler probes measured forearm skin blood flow-flux. Three THR tests were performed before and after heating skin for 5 min, and then after iontophoresis of norepinephrine 0.1%. Iontophoresis was pulsed using 45 s periods of 75 microA and 0 current over 10 min. Three temperatures were used: unheated skin, skin at 35 degrees C, and skin at 42 degrees C. Baseline flow-flux was measured for 60 s before each set of THR tests. THR ratio (THRR) was calculated by comparing baseline flow-flux immediately before arterial compression (F1) with the maximum after release (F2): THRR=F2/F1. The average values of each group of THRR results, and baseline data, were compared using the Kruskal-Wallis test. Iontophoresis of norepinephrine caused significant decreases in flow-flux (P<0.005). Unheated skin and skin heated to 35 degrees C showed significant decreases in THRR after norepinephrine. THRR was abolished by heating to 42 degrees C and partially restored by iontophoresis of norepinephrine. Iontophoresed norepinephrine causes vasoconstriction, and it partially restores vascular reactivity in the heat-induced vasodilated skin. This may be of benefit when norepinephrine is used in clinical situations.