The Modulating Effects of Sunscreen and Simulated Sweat on Ultraviolet Radiation‐ Induced Microvascular Dysfunction in the Human Cutaneous Vasculature
Authors: Wolf S. Tony , Stanhewicz Anna E , Jablonski Nina G , Ferguson Sara B , Kenney W. Larry 
Published: June 2021

After acute ultraviolet radiation (UVR) exposure, nitric oxide (NO)‐mediated vasodilation is attenuated in the cutaneous microvasculature, likely via increased oxidative stress. Application of sunscreen to the skin protects from, while sweat on the skin may exacerbate, deleterious effects of UVR, including the erythema. However, it is unknown whether the presence of sunscreen or sweat on the skin influences the effect of UVR exposure on NO‐dependent vasodilation, a marker of skin vascular health.

Purpose

To compare the impact of acute UVR, UVR with sunscreen (+SS), and UVR with simulated sweat (+SW) on NO‐mediated vasodilation in the cutaneous microcirculation. We hypothesized that +SS would blunt and +SW would augment the reduction in NO‐dependent vasodilation following acute UVR exposure.

Methods

Three intradermal microdialysis fibers were placed in the ventral skin of the left forearm and a single fiber was placed in the right forearm of 13 healthy adults (24±1 yr; 6M/7F) with mild to moderate skin pigmentation (M‐index 30–46). Sites on the left forearm were randomly assigned to UVR exposure (450 mJ/cm2), UVR+SS (SPF‐50 chemical sunscreen), or UVR+SW (64 mmol Na+, 2.1 mmol K+), while the sight on the right forearm served as a non‐UVR exposed control (CON). Following UVR exposure, a standardized local heating (42°C) protocol induced cutaneous vasodilation. After attaining a plateau blood flow, 15mM NG‐nitro‐L‐arginine methyl ester (L‐NAME; NO synthase inhibitor) was infused at all sites to quantify the NO contribution to cutaneous vasodilation. Red cell flux was measured at each site (laser‐Doppler flowmetry) and cutaneous vascular conductance (CVC=flux/MAP) was expressed as a percentage of maximum (%CVCmax; 28mM sodium nitroprusside+43°C) for each phase of the local heating response. The NO‐mediated contribution (%NO) was calculated as the difference between the local heating and L‐NAME plateaus.

Results

There were no differences in %CVCmax between treatments at baseline (p≥0.55), initial peak (p≥0.40), or heating plateau (p≥0.44). However, UVR blunted %NO compared to CON (CON: 40.8±4.8 vs UVR: 28.0±6.7%; p<0.01). The attenuation in %NO was prevented by sunscreen (UVR: 28.0±6.7 vs UVR+SS: 54.5±5.8%; p<0.01) and by simulated sweat (UVR: 28.0±6.7 vs UVR+SW: 45.8±5.2%; p<0.01). Further, when sunscreen was applied prior to UVR, UVR exposure actually augmented %NO compared to CON (UVR+SS: 54.5±5.8% vs CON: 40.8±4.8; p<0.01) or when sweat was on the skin (UVR+SS: 54.5±5.8 vs UVR+SW: 45.8±5.2%; p<0.01).

Conclusion

Acute broad spectrum UVR exposure attenuates NO‐mediated vasodilation in the cutaneous microvasculature. The presence of sunscreen or sweat on the skin may play a protective role against this effect, and UVR may actually augment NO‐mediated vasodilation in the presence of a chemical sunscreen.

Support or Funding Information

ACSM Foundation Doctoral Student Research Grant #17‐00552 and NIH T‐32 Grant #5T32AG049676‐03

This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.