Elevation of exhaled ethane concentration in asthma

被引:164
作者
Paredi, P [1 ]
Kharitonov, SA [1 ]
Barnes, PJ [1 ]
机构
[1] Natl Heart & Lung Inst, Dept Thorac Med, Imperial Coll Sch Sci Technol & Med, London SW3 6LY, England
关键词
D O I
10.1164/ajrccm.162.4.2003064
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
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, FEV1 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 +/- 0.70 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 FEV1 < 60% predicted value had higher concentrations of ethane (2.86 +/- 0.37 ppb) compared with less obstructed patients (FEV1 > 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.
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收藏
页码:1450 / 1454
页数:5
相关论文
共 35 条
[1]   Increased hydrogen peroxide and thiobarbituric acid-reactive products in expired breath condensate of asthmatic patients [J].
Antczak, A ;
Nowak, D ;
Shariati, B ;
Krol, M ;
Piasecka, G ;
Kurmanowska, Z .
EUROPEAN RESPIRATORY JOURNAL, 1997, 10 (06) :1235-1241
[2]  
AULIK I. V., 1966, BYUL EKSP BIOL MED, V62, P115
[3]   REACTIVE OXYGEN SPECIES AND AIRWAY INFLAMMATION [J].
BARNES, PJ .
FREE RADICAL BIOLOGY AND MEDICINE, 1990, 9 (03) :235-243
[4]   NEW CONCEPTS IN THE PATHOGENESIS OF BRONCHIAL HYPERRESPONSIVENESS AND ASTHMA [J].
BARNES, PJ .
JOURNAL OF ALLERGY AND CLINICAL IMMUNOLOGY, 1989, 83 (06) :1013-1026
[6]   INHIBITION BY METHYLPREDNISOLONE OF LEUKOCYTE-INDUCED PULMONARY DAMAGE [J].
CHIARA, O ;
GIOMARELLI, PP ;
BORRELLI, E ;
CASINI, A ;
SEGALA, M ;
GROSSI, A .
CRITICAL CARE MEDICINE, 1991, 19 (02) :260-265
[7]  
ENRIGHT PL, 1994, AM J RESP CRIT CAR S, V149, P9
[8]   SOURCE OF ETHANE IN EXPIRATE OF RATS VENTILATED WITH 100-PERCENT OXYGEN [J].
HABIB, MP ;
KATZ, MA .
JOURNAL OF APPLIED PHYSIOLOGY, 1989, 66 (03) :1268-1272
[9]   CIGARETTE-SMOKING AND ETHANE EXHALATION IN HUMANS [J].
HABIB, MP ;
CLEMENTS, NC ;
GAREWAL, HS .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 1995, 151 (05) :1368-1372
[10]   Effect of inhaled glucocorticoid on the cellular profile and cytokine levels in induced sputum from asthmatic patients [J].
Inoue, H ;
Aizawa, H ;
Fukuyama, S ;
Takata, S ;
Matsumoto, K ;
Shigyo, M ;
Koto, H ;
Hara, N .
LUNG, 1999, 177 (01) :53-62