Control of interstitial pneumonia by reducing nitric oxide production

放射性肺炎是放射治疗的主要并发症。为了阐明放射性肺炎的机制，我们研究了一氧化氮（NO）产生的肺组织使用单侧照射大鼠模型。我们的结果表明，照射后肺泡巨噬细胞（AM）产生NO，AM和肺泡上皮细胞中诱导型NO合酶（NOS）的表达增加。此外，放射性肺炎的进展与NOS抑制剂N^G-硝基-L-精氨酸甲酯（L-NAME）的体内治疗减少。L-NAME对肺组织Ⅲ型前胶原α 1 mRNA表达的抑制作用进一步证实。结果表明，AM和肺泡上皮细胞在照射后产生的NO可能是放射性肺炎发生发展的重要介质。数据的重现性是令人满意的，呼出气中CO浓度的估计被认为是适用于临床情况。

Radiation pneumonitis is a major complication of radiation therapy. To elucidate the mechanisms of radiation-induced pneumonitis, we studied nitric oxide (NO) produced from lung tissues using a model of unilaterally irradiated rats. Our results demonstrated that alveolar macrophages (AM) produced NO after irradiation, and the expression of inducible NO synthase (NOS) in both AM and alveolar epithelial cells was increased. Furthermore, the progression of radiation pneumonitis was reduced with the in vivo treatment of the NOS inhibitor N^G-nitro-L-arginine methyl ester (L-NAME). The effect of L-NAME was further confirmed by the inhibition of mRNA expression for procollagen-alpha_1 type III of the lung. With these results, NO produced from AM and alveolar epithelial cells after irradiation may be an important mediator in the progression of radiation pneumonitis.We measured CO concentration in expired air of healthy subjects. Reproducibility of the data was satisfactory and estimation of CO concentration in expired air was considered to be applicable in clinical situation.