OBJECT: Ultraviolet (UV) light irradiation can lead to immunomodulation. The purpose of this study was to determine the preventive effect of UV light on cerebral vasospasm by using a rabbit common carotid artery (CCA) model. METHODS: Rabbit CCAs were constricted for a long period by application of autologous blood within a silicon sheath. Before immersion in blood, the CCAs were adventitiously exposed to UV light emitted from a helium-cadmium laser (wavelength 325 nm) yielding an irradiation energy of 10 mJ/mm2. The occurrence of vasospasm was evaluated using angiography 48 hours after blood exposure in this model. The UV light treatment significantly reduced the degree of vasospasm. Compared with luminal diameters measured on Day 0, prior to treatment, the luminal diameters of UV light-treated arteries (six animals) decreased by only 6%, whereas that of the sham-treated arteries (eight animals) significantly decreased by 26% (p<0.001). Histological examination of UV light-treated CCAs revealed no endothelial damage and extended smooth-muscle cells, in which some fragmented nuclei were confirmed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling. Twenty-eight days after blood exposure, examination of UV light-treated CCAs revealed only myointimal proliferation, similar to that of the sham-treated CCAs. CONCLUSIONS: These results are the first to provide evidence of a prophylactic effect of UV light on vasospasm and are suggestive of involvement of apoptosis in the mechanism of this effect.
OBJECT: Ultraviolet (UV) light irradiation can lead to immunomodulation. The purpose of this study was to determine the preventive effect of UV light on cerebral vasospasm by using a rabbit common carotid artery (CCA) model. METHODS:Rabbit CCAs were constricted for a long period by application of autologous blood within a silicon sheath. Before immersion in blood, the CCAs were adventitiously exposed to UV light emitted from a helium-cadmium laser (wavelength 325 nm) yielding an irradiation energy of 10 mJ/mm2. The occurrence of vasospasm was evaluated using angiography 48 hours after blood exposure in this model. The UV light treatment significantly reduced the degree of vasospasm. Compared with luminal diameters measured on Day 0, prior to treatment, the luminal diameters of UV light-treated arteries (six animals) decreased by only 6%, whereas that of the sham-treated arteries (eight animals) significantly decreased by 26% (p<0.001). Histological examination of UV light-treated CCAs revealed no endothelial damage and extended smooth-muscle cells, in which some fragmented nuclei were confirmed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling. Twenty-eight days after blood exposure, examination of UV light-treated CCAs revealed only myointimal proliferation, similar to that of the sham-treated CCAs. CONCLUSIONS: These results are the first to provide evidence of a prophylactic effect of UV light on vasospasm and are suggestive of involvement of apoptosis in the mechanism of this effect.
Authors: K Nakai; T Kojima; K Hattori; S Miyachi; M Ishihara; N Kobayashi; T Okamoto; J Yoshida Journal: Interv Neuroradiol Date: 2008-05-15 Impact factor: 1.610