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。为了阐明辐射致肺炎的机制，我们使用单侧辐照大鼠模型研究了肺组织产生的一氧化氮（NO）。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合成酶（NOS）表达增加。此外，体内治疗NOS抑制剂N^ g -硝基- l -精氨酸甲酯（L-NAME）可减缓放射性肺炎的进展。L-NAME对III型肺原胶原α _1 mRNA表达的抑制进一步证实了其作用。这些结果表明，AM和肺泡上皮细胞在辐照后产生的NO可能是放射性肺炎进展的重要介质。我们测量了健康受试者过期空气中的CO浓度。数据的重现性令人满意，过期空气中CO浓度的估计可用于临床。

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.