Nitric oxide synthase inhibition attenuates cutaneous vasodilation during postmenopausal hot flash episodes.
Level 3 - non-randomized controlled study
Small within-subject controlled physiological experimental study in humans
PubMed 20505548 · doi:10.1097/gme.0b013e3181d674d6
What was done
Eight postmenopausal women (mean ± SD age, 51 ± 7 years) had four microdialysis membranes placed in their dorsal forearm skin. Each site received a different local infusion: Ringer solution (control), 10 mM ketorolac (prostaglandin inhibitor), 10 mM L-NAME (nitric oxide synthase inhibitor), or a combination of both. Skin blood flow was measured by laser-Doppler flowmetry during spontaneous hot flash episodes (13 episodes analyzed). Cutaneous vascular conductance (CVC) was expressed as a percentage of maximal CVC induced by 50 mM sodium nitroprusside.
What was found
Peak CVC increase at the control site was 15.5% ± 6% CVCmax. Ketorolac alone did not significantly alter peak CVC (13.0% ± 5% CVCmax; P = 0.09). In contrast, NOS inhibition significantly attenuated peak CVC at the L-NAME site (7.4% ± 4% CVCmax) and the L-NAME + ketorolac site (8.7% ± 7% CVCmax) relative to both control and ketorolac sites (P < 0.05 for both comparisons). Peak increase in sweat rate showed no significant difference among sites (P = 0.24).
Why it matters
The findings demonstrate that nitric oxide contributes substantially to the cutaneous vasodilation characterizing postmenopausal hot flashes, whereas prostaglandins do not appear to play a significant role.
Limits
The sample size was very small (8 women, 13 hot flash episodes). Vasodilation was assessed only in forearm skin and may not fully reflect responses in the face or chest. A substantial portion of the vasodilatory response persisted despite NOS inhibition, indicating other unidentified mechanisms.
Cited by
- contradicts Vasomotor hot flashes represent bodywide vascular spasms.