Kelfkens G, van Helden A C, van der Leun J C
University of Utrecht, Institute of Dermatology, Utrecht, The Netherlands.
Photodermatol Photoimmunol Photomed. 1990 Aug;7(4):178-82.
Measurement of the change in skin temperature caused by exposure of the skin to ultraviolet (UV) radiation may give insight into the mechanism responsible for the development of the UV erythema. Under controlled environmental conditions we determined the temperature change of skin areas exposed to UVA, up to 24 h after irradiation. The UVA doses given were 3 or 4 times the minimal erythema dose (MED). The 3-MED and the 4-MED doses resulted in elevation of skin temperature. Delayed UVA erythema was accompanied by skin temperature rise, indicating involvement of arteriolar vessels in the UVA erythema. This arteriolar dilation is best explained if we assume that the delayed erythema is caused by a vasoactive mediator, most likely released in the epidermis, which reaches the dermal blood vessels by diffusion. This result, combined with earlier studies, leads to the conclusion that the erythemas elicited by UVA, UVB and UVC are probably all brought about by diffusing mediators, and not by direct action of the radiation on the blood vessels.
测量皮肤暴露于紫外线(UV)辐射后引起的皮肤温度变化,可能有助于深入了解导致紫外线红斑形成的机制。在可控的环境条件下,我们测定了暴露于UVA的皮肤区域在照射后长达24小时的温度变化。给予的UVA剂量为最小红斑剂量(MED)的3倍或4倍。3-MED和4-MED剂量导致皮肤温度升高。延迟性UVA红斑伴有皮肤温度升高,表明小动脉血管参与了UVA红斑的形成。如果我们假设延迟性红斑是由一种血管活性介质引起的,这种介质很可能在表皮中释放,并通过扩散到达真皮血管,那么这种小动脉扩张就最容易解释了。这一结果与早期研究相结合,得出的结论是,UVA、UVB和UVC引起的红斑可能都是由扩散性介质引起的,而不是辐射对血管的直接作用。