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J Appl Physiol 94: 227-233, 2003. First published September 13, 2002; doi:10.1152/japplphysiol.00551.2002
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Vol. 94, Issue 1, 227-233, January 2003

Desiccation and hypertonicity of the airway surface fluid and thermally induced asthma

Chakradhar Kotaru, Rana B. Hejal, J. H. Finigan, Albert J. Coreno, Mary E. Skowronski, Lori Brianas, and E. R. McFadden Jr.

General Clinical Research Center of Case Western Reserve University School of Medicine and Division of Pulmonary and Critical Care Medicine and Department of Medicine of University Hospitals of Cleveland, Cleveland 44106; and MetroHealth Medical Center, Cleveland, Ohio 44109-1998

To determine whether drying and hypertonicity of the airway surface fluid (ASF) are involved in thermally induced asthma, nine subjects performed isocapnic hyperventilation (HV) (minute ventilation 62.2 ± 8.3 l/min) of frigid air (-8.9 ± 3.3°C) while periciliary fluid was collected endoscopically from the trachea. Osmolality was measured by freezing-point depression. The baseline 1-s forced expiratory volume was 73 ± 4% of predicted and fell 26.4% 10 min postchallenge (P > 0.0001). The volume of ASF collected was 11.0 ± 2.2 µl at rest and remained constant during and after HV as the airways narrowed (HV 10.6 ± 1.9, recovery 6.5 ± 1.7 µl; P = 0.18). The osmolality also remained stable throughout (rest 336 ± 16, HV 339 ± 16, and recovery 352 ± 19 mosmol/kgH2O, P = 0.76). These data demonstrate that airway desiccation and hypertonicity of the ASF do not develop during hyperpnea in asthma; therefore, other mechanisms must cause exercise- and hyperventilation-induced airflow limitation.

airway drying; hyperpnea; bronchoconstriction


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