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

摘要

BACKGROUND: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.