Photosynthesis of previtamin D3 can occur throughout the epidermis in the dermis when hypopigmented Caucasian skin is exposed to solar ultraviolet radiation. Once previtamin D3 is formed in the skin, it undergoes a temperature-dependent thermal isomerization that takes at least 3 days to complete. The vitamin D-binding protein preferentially translocates the thermal product, vitamin D3, into the circulation. These processes suggest a unique mechanism for the synthesis, storage, and slow, steady release of vitamin D3 from the skin into the circulation.
On the basis of models describing optical and thermal transfer in tissue, it has been shown that unfocused, pulsed 577-nm laser irradiation of human skin selectively damages microvessels with little or no direct damage to other tissue structures such as the epidermis. This is in sharp contrast to the histologically nonselective necrosis induced by continuous lasers, in which essentially all structures near the site of exposure are damaged. We report here preliminary data in an animal model regarding mechanisms by which tunable dye lasers selectively alter blood and microvasculature. Irradiations of the hamster cheek pouch were used for direct microscopic observations of immediate changes in vessel integrity and morphology, and in the appearance and flow of blood. In 20- to 100-micron-diameter vessels, a sequence of brown discoloration and viscidification of blood, transient hemostasis, permanent hemostasis, and hemorrhage were observed with increasing exposure doses.
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