Nitric Oxide Inhibition Attenuates Cutaneous Vasodilation During The Post-menopausal Hot Flash.

Abstract

PURPOSE: The purpose of this study was to test the hypothesis that local inhibition of nitric oxide and prostaglandin synthesis would attenuate cutaneous vasodilator responses during post-menopausal hot flashes. METHODS: Four microdialysis membranes were inserted into forearm skin (dorsal surface) of 8 post-menopausal women (51±7 yrs). Ringers solution (control), 10mM Ketorolac (Keto), 10mM NG-l-arginine methyl ester (L-NAME), and a combination of 10mM Keto + 10mM L-NAME were each infused at the separate sites. Skin blood flow at each site was indexed using laser-Doppler flowmetry. The onset of a flash was defined as an increase of 0.002 mg/cm-2·minute-1 per second in sternal sweat rate (capacitance hygrometry). Cutaneous vascular conductance (CVC) was calculated as laser-Doppler flux/mean arterial pressure. CVC is expressed as a percentage of the maximal calculated CVC (CVCmax) obtained following infusion of 50mM sodium nitropruside at all sites at the end of the study. RESULTS: Data from 13 hot flashes were analyzed. At the control site, the mean peak increase in CVC was 14±5% CVCmax units. This value was not different relative to the peak increase in CVC at the Keto site (15±7% CVCmax units, P=0.77). However, the peak increase in CVC during the flash was attenuated at the L-NAME and L-NAME+Keto sites (7±4% CVCmax units and 8±7% CVCmax units, respectively, P<0.05 for both sites) relative to both the control and the Keto sites. There was no difference in sweat rate between any of the sites (P=0.99). CONCLUSION: These data demonstrate that cutaneous vasodilation during a hot flash has a nitric oxide component. Increases in CVC despite the inhibition of prostaglandin synthesis suggest prostaglandins do not contribute to cutaneous vasodilation during a hot flash. Supported by NIH Grant AG030189.