| pubmed-article:7341895 | pubmed:abstractText | Basic theoretical considerations of the optical and thermal transfer processes that govern the thermal damage induced in tissue by lasers are discussed. An approximate, predictive model and data are proposed for the purpose of selecting a laser that maximizes damage to cutaneous blood vessels and minimizes damage to the surrounding connective tissue and the overlying epidermis. The variables of wavelength, exposure duration, and incident energy density are modeled, and a flashlamp-pumped dye laser operating at or near the 577 nm absorption band of HbO2, with a pulse width (0.3 microsecond) less than the estimated, approximately 1 millisecond, thermal relaxation times for microvessels is chosen for experimental exposures of normal Caucasian skin. Highly specific laser-induced damage to blood vessels is demonstrated both clinically and histologically. This is in striking contrast to the previously reported widespread, diffuse necrosis caused by other lasers. The incident energy and preliminary observations of wavelength and temperature dependence for vascular damage thresholds are consistent with theoretical predictions. Whereas typically 20 joules/cm2 of argon laser irradiation (514 and 488 nm, approximately 100 msec) is required to induce widespread thermal damage, the pulsed dye laser requires only about 2 joules/cm2 to induce highly specific vascular damage. The potential usefulness of dye laser-induced selective vascular damage as a treatment modality for portwine stain hemangiomas and other vascular lesions is discussed. In addition to possible treatment applications, the dye laser or other sources meeting the requirements for producing such damage may also offer a useful experimental tool for inducing predictable damage to microvasculature. Histopathologic and clinical studies related to these possibilities are in progress. | lld:pubmed |
