Journal of Applied Physiology
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J Appl Physiol (September 13, 2002). doi:10.1152/japplphysiol.00551.2002
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Articles in PresS, published online ahead of print September 13, 2002
J Appl Physiol, 10.1152/jap.00551.2002
Submitted on June 25, 2002
Accepted on September 4, 2002

Desiccation and Hypertonicity of the Airway Surface Fluid and Thermally Induced Asthma

Chakradhar Kotaru1, Rana B Hejal2, James H Finigan2, Albert J Coreno2, Mary E Skowronski2, Lori J Brianas2, and E. R McFadden, Jr.2*

1 Division of Pulmonary and Critical Care Medicine, University of Colorado School of Medicine, Denver, CO, USA
2 School of Medicine, Case Western Reserve University, Cleveland, OH, USA

* To whom correspondence should be addressed. E-mail: erm2{at}po.cwru.edu.

To determine if drying and hypertonicity of the airway surface fluid (ASF) is involved in thermally induced asthma, 9 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 one second forced expiratory volume (FEV1) was 73 ± 4% of predicted and fell 26.4 % 10 minutes post challenge (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 mOsm/l, P = 0.76). These data demonstrate that airway desiccation and hypertonicity of the ASF do not develop during hyperpnea in asthma; therefore, other mechanism must cause exercise and hyperventilation induced airflow limitation.




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