Red light mediated vasodilation (698.12)

Abstract

Over 8 million Americans are treated for symptoms related to peripheral artery disease (PAD). Risk factors for PAD have been directly related to a reduction in NOS expression and NO production. Light irradiation at the far red/near infrared region (670 nm (R/NIR)) can stimulate angiogenesis by increasing NO independent of NOS through release of NO from nitrosyl‐heme stores. We hypothesized R/NIR can stimulate vasodilation, and serve as a potential therapy to improve endothelial function. Methods: Human umbilical vein endothelial cells (HUVEC) were loaded with DAF‐2 and stimulated with R/NIR at 25mW, 50mW, and 75mW up to 12J. NO was measured using HPLC of DAF‐2T. Facial arterioles from c57Bl/6 mice and human coronary arterioles from patients with and without atherosclerosis were pressurized to 60mmHg and pre‐constricted. Vessels were irradiated with 670 nm light (10mW/cm2) up to 5 min at a time with 10 min dark period between irradiation. Results: R/NIR stimulated a 26.83% (± 6.99, p<0.05) increase in NO over control. Preincubation with c‐PTIO, a NO scavenger, completely abolished R/NIR stimulated NO. In mice, vessel diameter increased 17.8% (±3.0, p<0.05) after R/NIR exposure. In vessels denuded prior to R/NIR dilation, vasodilation was abolished (1.2%, ± 2.21, p<0.001), suggesting R/NIR vasodilation was endothelial dependent. Pre‐incubation with 1mM L‐NAME did not significantly attenuate dilation (13.74% ±2.2), however c‐PTIO (100µM) could successfully block dilation (‐.51% ± 1.1, p<0.001). R/NIR significantly increased in coronary arterioles from patients with atherosclerosis 24.5% (±2.1%, p<0.01) and without atherosclerosis 44.8% (±6.2%, p<0.01). Conclusion: R/NIR can stimulate vasodilation in human and murine vessels. This vasodilation is endothelium and NO dependent, but does not require functional nitric oxide synthase. The exact source for the NO increase is unknown, but intracellular nitrosyl heme moieties should be considered as a previously unexplored source for NO.