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

机译:体内脉冲紫外线照射引起的血管松弛:光化学一氧化氮和光声波效应的参与

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Abstract: 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. !9
机译:摘要:我们研究了光化学一氧化氮在紫外线脉冲光诱导的血管舒张中的参与。我们在氟化K(KrF)受激准分子激光辐照期间测量了体内大鼠股动脉的腔直径。我们还测量了亚硝酸钠,超氧化物歧化酶或亚甲蓝对动脉进行预处理时的血管反应。通过光学显微镜检查血管的组织学变化。 KrF激光使血管松弛。在恒定总能量下,血管舒张依赖于重复率。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理引起的。亚甲基蓝抑制血管舒张,但亚硝酸钠或超氧化物歧化酶则增强血管舒张,这强烈表明松弛与一氧化氮密切相关。我们得出结论,一氧化氮的光化学产物可能是脉冲紫外线诱发血管舒张的可能机制之一。 !9

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