Paredi P, Kharitonov S A, Barnes P J
Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College School of Science, Technology and Medicine, London, United Kingdom.
Am J Respir Crit Care Med. 2000 Oct;162(4 Pt 1):1450-4. doi: 10.1164/ajrccm.162.4.2003064.
Ethane is a product of lipid peroxidation as a result of oxidative stress and can be detected in the exhaled air. Oxidative stress plays a role in the pathogenesis of asthma. We measured exhaled ethane in 26 asthmatic subjects (mean age +/- SEM, 38 +/- 8 yr; 15 male, FEV(1) 60 +/- 4%) and compared it with exhaled nitric oxide (NO) measured by chemiluminescence, a noninvasive marker of oxidative stress and inflammation. Exhaled ethane was collected during a flow- and pressure-controlled exhalation into a reservoir discarding dead space air contaminated with ambient air. A sample of the expired air was analyzed by chromatography. Exhaled ethane levels were elevated in asthma patients not receiving steroid (n = 12, 2.06 +/- 0.30 ppb) compared with steroid-treated patients (n = 14, 0.79 +/- 0.10 ppb, p < 0.01) and to 14 nonsmoking control subjects (0.88 +/- 0.09 ppb, p < 0.05). In patients not receiving steroid treatment there was a positive correlation between exhaled ethane and NO (r = 0.55, p < 0.05) and air trapping assessed by the ratio of residual volume to total lung capacity (RV/ TLC) (r = 0.60, p < 0.05). In addition, untreated patients with FEV(1) < 60% predicted value had higher concentrations of ethane (2.86 +/- 0.37 ppb) compared with less obstructed patients (FEV(1) > 60%, 1.26 +/- 0.12 ppb, p < 0.05). NO concentrations were higher in patients not on steroid treatment (14.7 +/- 1.7 ppb) than in steroid-treated patients (8.6 +/- 0.5 ppb, p < 0.05). Exhaled ethane is elevated in asthma, reduced in steroid-treated patients, and correlates with NO and airway obstruction. It may be a useful noninvasive marker of oxidative stress.
乙烷是氧化应激导致脂质过氧化的产物，可在呼出气体中检测到。氧化应激在哮喘发病机制中起作用。我们测量了26名哮喘患者（平均年龄±标准误，38±8岁；15名男性，第1秒用力呼气容积[FEV(1)]为60±4%）呼出的乙烷，并将其与通过化学发光法测量的呼出一氧化氮（NO）进行比较，NO是氧化应激和炎症的一种非侵入性标志物。在流量和压力控制的呼气过程中，将呼出的乙烷收集到一个储器中，弃去被环境空气污染的死腔空气。用色谱法分析呼出气体的一个样本。未接受类固醇治疗的哮喘患者（n = 12，2.06±0.30 ppb）呼出的乙烷水平高于接受类固醇治疗的患者（n = 14，0.79±0.10 ppb，p < 0.01）以及14名非吸烟对照者（0.88±0.09 ppb，p < 0.05）。在未接受类固醇治疗的患者中，呼出的乙烷与NO之间存在正相关（r = 0.55，p < 0.05），且与通过残气量与肺总量之比（RV/TLC）评估的气体潴留存在正相关（r = 0.60，p < 0.05）。此外，预测FEV(1) < 60%的未治疗患者的乙烷浓度（2.86±0.37 ppb）高于阻塞程度较轻的患者（FEV(1) > 60%，1.26±0.12 ppb，p < 0.05）。未接受类固醇治疗的患者的NO浓度（14.7±1.7 ppb）高于接受类固醇治疗的患者（8.6±0.5 ppb，p < 0.05）。哮喘患者呼出的乙烷升高，接受类固醇治疗的患者降低，且与NO和气道阻塞相关。它可能是氧化应激的一种有用的非侵入性标志物。
