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Am. J. Respir. Crit. Care Med., Volume 165, Number 3, February 2002, 332-337

Increased Nitric Oxide Output from Alveolar Origin during Liver Cirrhosis versus Bronchial Source during Asthma

CHRISTOPHE DELCLAUX, BRUNO MAHUT, FRANÇOISE ZERAH-LANCNER, CHRISTOPHE DELACOURT, SYLVA LAOUD, DANIEL CHERQUI, CHRISTOPHE DUVOUX, ARIANE MALLAT, and ALAIN HARF

Service de Physiologie-Explorations Fonctionnelles, Service d'Hépato-Gastroentérologie, Consultation d'Allergologie, Service de Chirurgie Digestive, Hôpital Henri Mondor, Créteil, Assistance Publique-Hôpitaux de Paris, Service de Pédiatrie, Centre Hospitalier Intercommunal de Créteil, and Unité INSERM U 492-Université Paris XII, Faculté de Médecine de Créteil, Créteil, France

The aim of this study was to assess the usefulness of nitric oxide (NO) output measurement at multiple expiratory flow rates during diseases characterized by increased exhaled NO (FENO) that could come from alveolar (liver cirrhosis) or bronchial (asthma) sources. It has been proposed that NO output measurements expressed as a function of expiratory flow allow alveolar NO concentration (FANO) and maximal bronchial NO output (Qbr,max NO) to be computed. In 36 healthy nonsmoking subjects, we found that maximal bronchial NO output (37 ± 3 nl/min) was correlated with the height of the subjects (p = 0.02). Alveolar NO concentration was 5.1 ± 0.3 (SEM) ppb, which represented 31 ± 2% and 61 ± 3% of FENO at 50 and 200 ml/s expiratory flow rate, respectively. Nonsmoking subjects with asthma (n = 28) were characterized by an increase in Qbr,max NO (133 ± 14 nl/min) as compared with healthy nonsmoking subjects (p < 0.0001). FENO50, FENO200, and Qbr,max NO were equally efficient in differentiating subjects with asthma from healthy subjects. Patients with liver cirrhosis (n = 26, 14 smokers and 12 nonsmokers) had an increased FANO compared with healthy subjects (cirrhosis: 8.3 ± 0.9 ppb, healthy nonsmokers [n = 36] and smokers [n = 20], n = 56: 4.7 ± 0.3 ppb, p < 0.05), which was correlated with the alveolar-arterial oxygen difference (p = 0.007). FANO and FENO200, but not FENO50 values, allowed patients with liver cirrhosis to be differentiated from healthy subjects. These results suggest that a two-compartment model for NO output allows the increase in FENO from alveolar sources to be differentiated from the increase from bronchial sources.




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