Shinkai Masaharu, Suzuki Shunsuke, Miyashita Akira, Kobayashi Hideo, Okubo Takao, Ishigatsubo Yoshiaki
First Department of Internal Medicine, Yokohama City University School of Medicine, Yokohama, Japan.
Chest. 2002 Jun;121(6):1847-52. doi: 10.1378/chest.121.6.1847.
The precise anatomic sites contributing to exhaled nitric oxide (eNO) are still unknown. The present study was designed to analyze profiles of eNO by referring to the He exhalation curve and examining the effects of breath-holding and expiratory flow rates on eNO.
Healthy volunteers and patients with stable asthma. MEASUREMENTS AND RESULTS We used the He bolus method of the closing volume, and simultaneously analyzed the concentrations of exhaled He and nitric oxide (NO). By referring to the He exhalation curve, the expired gas was divided into three parts: airway dead space (phase 1), a mixture of airway and alveolar gas (phase 2), and alveolar gas (phase 3 and phase 4). The eNO profiles showed a peak in phase 2 (peak eNO) and decreased gradually to a plateau in the latter half of phase 3 (plateau eNO). The levels of peak eNO were higher than those of plateau eNO in both normal subjects and asthmatic patients. Breath-holding increased levels of peak eNO 2.5-fold in both normal subjects and asthmatic patients, but it did not affect the levels of plateau eNO. The levels of peak eNO increased as the expiratory flow rate decreased, and the levels of plateau eNO showed a similar flow dependency.
A peak value of eNO concentration profiles may directly express the production of NO in the airway.
