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近年发现哮喘患者及动物模型呼出气中含有高浓度的一氧化氮(NO)。根据免疫组化及原位杂交技术证明哮喘发作时气道上皮及炎症浸润细胞内NO合成酶mRNA增加,NO合成酶活性增强。吸入糖皮质激素治疗可使哮喘患者呼出气中NO降至正常,呼出气NO增多可能是气道炎症的反映,监测呼出气中NO浓度可作为哮喘发作及其严重程度的指际。吸入高浓度NO可降低气道阻力,NO对去上皮的豚鼠气管环具有强烈的舒张作用,但NO扩张气道粘膜血管,增强渗出,诱发气道粘膜水肿,通过非肌性机制加重气道阻塞。NO还通过凋节T淋巴细胞免疫增强气道炎症反应。NO在哮喘发病中的作用尚不清楚,其机制的阐明将有助于哮喘的治疗。
In recent years, asthma patients and animal models have been found to contain high concentrations of nitric oxide (NO) in the exhaled breath. According to immunohistochemistry and in situ hybridization, the NO synthase mRNA and the activity of NO synthase were increased in the airway epithelium and inflammatory infiltrating cells. Inhaled glucocorticoid therapy can exacerbate NO in exhaled breath of asthmatic patients, increased exhaled breath of NO may be a reflection of airway inflammation, and monitoring of NO concentration in exhaled breath may be used as an index of asthma attacks and their severity. Inhalation of high concentrations of NO can reduce airway resistance, nitric oxide detrusor guinea pig tracheal ring has a strong diastolic function, but NO expansion of airway mucosal blood vessels, enhance exudation, induced airway mucosal edema, increased non-muscular mechanism of airway block. NO also enhances airway inflammation through apoptosis of T lymphocytes. The role of NO in the pathogenesis of asthma is unclear, and the elucidation of its mechanism will contribute to the treatment of asthma.