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Vasorelaxation induced by pulsed ultraviolet light irradiation in vivo: involvement of photochemical nitric oxide and photoacoustic wave effect

机译:脉冲紫外光辐照诱导的血管插入体内:光化学一氧化氮和光声波效应的累积

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We examined a participation of photochemical nitric oxide in the vasorelaxation induced by ultraviolet pulsed light. We measured a luminal diameter of rat femoral artery in vivo during a Krypton-fluoride (KrF) excimer laser irradiation. We also measured the vascular response when the artery was pretreated with sodium nitrite, superoxide dismutase or methylene blue. Histological changes in the vessels were examined by light microscopy. The vessel relaxed by KrF laser. The vasorelaxation was dependent on the repetition rate under the constant total energy. On the contrary, the vessel wall damage was inversely proportional to the repetition rate. Accordingly, the damage is most likely due to photoacoustic mechanism. The vasorelaxation was inhibited by methylene blue but enhanced by sodium nitrite or superoxide dismutase, which strongly suggests that the relaxation is closely related to nitric oxide. We conclude that the photochemical product of nitric oxide may be one of the possible mechanisms for the pulsed ultraviolet light induced vasorelaxation.
机译:我们研究了光化学一氧化氮在紫外线脉冲光诱导的血管内氧化物中的参与。在氪 - 氟化物(KRF)准分子激光照射期间,我们在体内测量了大鼠股动脉的腔直径。当用亚硝酸钠,超氧化物歧化酶或亚甲基蓝色预处理动脉时,我们还测量了血管反应。通过光学显微镜检查血管中的组织学变化。通过KRF激光弛豫的血管。血管插入依赖于恒定总能量下的重复率。相反,血管壁损伤与重复率成反比。因此,损坏很可能是由于光声机制。通过亚甲基蓝色抑制血管加速,但通过亚硝酸钠或超氧化物歧化酶增强,这强烈表明松弛与一氧化氮密切相关。我们得出结论,一氧化氮的光学化学产物可以是脉冲紫外线诱导的血管内膨胀的可能机制之一。

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