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1Fisiopatologia Respiratoria and 8Terapia Intensiva Cardiochirurgica, Azienda Ospedaliera S. Croce e Carle, 12100 Cuneo; 2Dipartimento di Bioingegneria, Politecnico, 20133 Milano; 3Centro di Bioingegneria, Fondazione Don Gnocchi Instituto di Ricovero e Cura a Carattere Scientifico, 20148 Milano; 5UOF di Riabilitazione Respiratoria, Fondazione Don C. Gnocchi "ONLUS," 50020 Pozzolatico; 6Dipartimento di Medicina Interna, Università di Firenze, 50134 Florence; 7Centro Cardiologico Monzino Istituto di Ricovero e Cura a Carattere Scientifico, Istituto di Cardiologia, Università di Milano, 20122 Milano; and 9Dipartimento di Medicina Interna, Università di Genova, 16132 Genoa, Italy; and 4Meakins Christie Laboratories and McGill University, Montreal, Canada H3A 2T5
Submitted 26 March 2003 ; accepted in final form 30 April 2003
Lung mechanics and airway responsiveness to methacholine (MCh) were studied
in seven volunteers before and after a 20-min intravenous infusion of saline.
Data were compared with those of a time point-matched control study. The
following parameters were measured: 1-s forced expiratory volume, forced vital
capacity, flows at 40% of control forced vital capacity on maximal
(
m40) and partial
(
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 and also at different lung volumes above and below
functional residual capacity. Rrs was measured at functional residual capacity
and at total lung capacity. Before MCh, saline infusion caused significant
decrements of forced expiratory volume in 1 s,
m40, and
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
m40 to
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 deep inhalation. It is speculated that
it was likely the result of airway wall edema encroaching on the bronchial
lumen.
lung elastic recoil; pulmonary resistance; dynamic elastance; methacholine challenge; deep inhalation
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