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1 Fisiopatologia Respiratoria, Azienda Ospedaliera S. Croce e Carle, Cuneo, Italy
2 Dipartimento di Bioingegneria, Politecnico di Milano, Milano, Italy; Centro di Bioingegneria, Fondazione Don Gnocchi, Milano, Italy
3 Meakins Christie Laboratories, McGill University, Montreal, Canada
4 Riabilitazione Respiratoria, Fondazione Don Gnocchi, Pozzolatico, Italy
5 Dipartimento di Medicina Interna, Universita' di Firenze, Firenze, Italy
6 Centro Cardiologico Monzino IRCCS, Istituto di Cardiologia, Universita' di Milano, Milano, Italy
7 Terapia Intensiva Cardiochirurgica, Azienda Ospedaliera S. Croce e Carle, Cuneo, Italy
8 Dipartimento di Medicina Interna, Universita' di Genova, Genova, Italy
* To whom correspondence should be addressed. E-mail: Vito.Brusasco{at}unige.it.
Lung mechanics and airway responsiveness to methacholine (MCh) were studied in 7 volunteers before and after a 20-min intravenous infusion of saline. Data were compared with those of a time-points matched control study. The following parameters were measured: 1-s forced expiratory volume (FEV1), forced vital capacity (FVC), flows at 40% of control FVC on maximal (V m40) and partial (V p40) forced expiratory maneuvers, lung volumes, lung elastic recoil, lung resistance (RL), dynamic elastance (Edyn), and within-breath resistance of respiratory system (Rrs). RL and Edyn were measured during tidal breathing before and for 2 min after a deep inhalation (DI), and also at different lung volumes above and below functional residual capacity (FRC). Rrs was measured at FRC and at total lung capacity. Before MCh, saline infusion caused significant decrements of FEV1, V m40, and V p40, but insignificantly affected lung volumes, elastic recoil, RL, Edyn, and Rrs at any lung volume. Furthermore, saline infusion was associated with an increased response to MCh, which was not associated with significant changes in the ratio of V m40/V p40. In conclusion, mild airflow obstruction and enhanced airway responsiveness were observed after saline, but this was not apparently due to altered elastic properties of the lung or inability of the airways to dilate with DI. It is speculated that it was likely the result of airway wall edema encroaching on the bronchial lumen.
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