Light-induced vasodilation of coronary arteries and its possible clinical implication.

BACKGROUND: Low-level laser therapy and light-emitting diodes (LED) are increasingly used in phototherapy. Their therapeutic effects are at least partly mediated by light-induced vasodilation. The aim of this study was to determine the effect of different light sources on coronary arteries.
METHODS: Porcine left coronary arteries were cut into 4-mm rings that were irradiated either by a semiconductor nonthermal gallium-arsenide diode laser or a noncoherent athermic red light source both with the same energy density up to 16 J/cm(2). After precontraction with 9, 11-dideoxy-11α, 9α-epoxymethano-prostaglandin F(2)α, respective relaxation responses were evaluated. The role of endothelium as well as intracellular pathways was investigated.
RESULTS: Maximum vasodilation after exposure to laser was observed at 10 J/cm(2) (56.8% ± 1.2%) and decreased to 43.9% ± 2.8% at 16 J/cm(2) (p < 0.003). After adjusting exposure time to achieve equivalent energy densities in the LED group, vessel segments revealed photorelaxation of 52.9% ± 6.5% and 47.5% ± 0.6%, respectively. Vasodilations achieved by either light source were comparable at 10 J/cm(2) (p < 0.574) and 16 J/cm(2) (p < 0.322). Furthermore, vasodilation could be inhibited by administration of 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (nitric oxide scavenger) and 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (guanocyclase inhibitor) but not with L-nitro-arginine methyl ester or deendothelialization.
CONCLUSIONS: Vessels exposed to either light source showed a remarkable as well as comparable photorelaxation at definite energy densities. This effect is mediated by an intracellular nitric oxide-dependent mechanism. As LED sources are of small size, simple, and inexpensive build-up, they may be used during routine coronary artery bypass surgery to ease suturing of anastomosis by target vessel vasodilation.