Sunscreen or simulated sweat minimizes the impact of acute ultraviolet radiation on cutaneous microvascular function in healthy humans

Abstract

New findings: What is the central question of this study? Are ultraviolet radiation (UVR)-induced increases in skin blood flow independent of skin erythema? Does broad-spectrum UVR exposure attenuate NO-mediated cutaneous vasodilatation, and does sunscreen or sweat modulate this response? What are the main findings and their importance? Erythema and vascular responses to UVR are temporally distinct, and sunscreen prevents both responses. Exposure to UVR attenuates NO-mediated vasodilatation in the cutaneous microvasculature; sunscreen or simulated sweat on the skin attenuates this response. Sun over-exposure may elicit deleterious effects on human skin that are separate from sunburn, and sunscreen or sweat on the skin may provide protection.

Abstract: Exposure to ultraviolet radiation (UVR) may result in cutaneous vascular dysfunction independent of erythema (skin reddening). Two studies were designed to differentiate changes in erythema from skin vasodilatation throughout the 8 h after acute broad-spectrum UVR exposure with (+SS) or without SPF-50 sunscreen (study 1) and to examine NO-mediated cutaneous vasodilatation after acute broad-spectrum UVR exposure with or without +SS or simulated sweat (+SW) on the skin (study 2). In both studies, laser-Doppler flowmetry was used to measure red cell flux, and cutaneous vascular conductance (CVC) was calculated (CVC = flux/mean arterial pressure). In study 1, in 14 healthy adults (24 ± 4 years old; seven men and seven women), the skin erythema index and CVC were measured over two forearm sites (UVR only and UVR+SS) before, immediately after and every 2 h for 8 h post-exposure (750 mJ cm^-2 ). The erythema index began to increase immediately post-UVR (P < 0.05 at 4, 6 and 8 h), but CVC did not increase above baseline for the first 4-6 h (P ≤ 0.01 at 6 and 8 h); +SS prevented both responses. In study 2, in 13 healthy adults (24 ± 4 years old; six men and seven women), three intradermal microdialysis fibres were placed in the ventral skin of the forearm [randomly assigned to UVR (450 mJ cm^-2 ), UVR+SS or UVR+SW], and one fibre (non-exposed control; CON) was placed in the contralateral forearm. After UVR, a standardized local heating (42°C) protocol quantified the percentage of NO-mediated vasodilatation (%NO). The UVR attenuated %NO compared with CON (P = 0.01). The diminished %NO was prevented by +SS (P < 0.01) and +SW (P < 0.01). Acute broad-spectrum UVR attenuates NO-dependent dilatation in the cutaneous microvasculature, independent of erythema. Sunscreen protects against both inflammatory and heating-induced endothelial dysfunction, and sweat might prevent UVR-induced reductions in NO-dependent dilatation.

Keywords: endothelial function; nitric oxide; sun safety; ultraviolet radiation.

Figure 1

Schematic of the local heating protocol (study 2) with a representative tracing of laser-doppler flux. Prior to UVR exposure, microdialysis sites on the left forearm were randomized for UVR exposure alone, UVR with sunscreen applied to the skin (UVR+SS), or UVR with simulated sweat applied to the skin (UVR+SW). A single site on the right forearm acted as a non-exposed control. After UVR exposure, each site was locally heated to 42°C to elicit an increase in blood flow. After a local heating plateau was observed, L-NAME was perfused through all sites to inhibit nitric oxide synthase. The arrow indicates the decrease with L-NAME infusion used to calculate %NO-dependent dilation. The experiment concluded with perfusion of sodium nitroprusside and local heat increased to 43°C at all sites to elicit maximal vasodilation.

Figure 2

Changes in erythema index (left) and cutaneous vascular conductance (right) after exposure to UVR only (open circles) or UVR with sunscreen applied to the skin (closed circles). Values are mean ± SD. * P < 0.05 compared to baseline; § P < 0.05 compared to UVR only; n=14.

Figure 3

Cutaneous vascular conductance (%CVCmax) at each phase of the local heating protocol in the non-exposed control site (- UVR; white bar) or after UVR exposure alone (+ UVR; gray bar), with sunscreen on the skin (+ UVR + SS; hashed bar), or with simulated sweat on the skin (+ UVR + SW; light gray bar). Values are mean ± SD. * P < 0.05 compared to (−) UVR; ‡ P < 0.05 compared to (+) UVR; n=13.

Figure 4

Differences in percent contribution of nitric oxide (NO) to the local heating plateau in (A) the non-exposed control site (- UVR; white bar) vs. UVR exposure alone (+ UVR; gray bar), (B) UVR exposure alone (+ UVR; gray bar) vs. UVR with sunscreen on the skin (+ UVR + SS; hashed bar), or (C) UVR exposure alone (+ UVR; gray bar) vs. UVR with simulated sweat on the skin (+ UVR + SW; light gray bar). Data are presented as means with individual responses illustrated by connecting lines. * P < 0.05 between treatments; n=13.