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Am. J. Respir. Crit. Care Med., Volume 163, Number 2, February 2001, 383-388

Exhaled Nitric Oxide and Thermally Induced Asthma

CHAKRADHAR KOTARU, ALBERT CORENO, MARY SKOWRONSKI, RUSSELL CIUFO, and E. R. MCFADDEN Jr.

Division of Pulmonary and Critical Care Medicine and the Airway Disease Center of University Hospitals of Cleveland, and the Department of Medicine of Case Western Reserve University School of Medicine, Cleveland, Ohio

The purpose of the present study was to determine if nitric oxide (NO) is involved in the pathogenesis of thermally induced asthma. To provide data on this issue, 10 normal and 13 asthmatic subjects performed isocapnic hyperventilation with frigid air while the fractional concentration of NO in the expirate air (FENO) was serially monitored with a chemiluminescence analyzer. FEV1 was measured before and after hyperpnea. Prior to and throughout the challenge, the asthmatics had significantly larger values for FENO (baseline FENO normal, 11 ± 2 ppb; asthma, 16 ± 1; p = 0.03). Posthyperpnea, the normal subjects had little change in bronchial caliber (Delta FEV1 baseline to 5 min posthyperpnea, -3.5 ± 1.5%; p = 0.06), whereas the patients with asthma developed significant airway obstruction (Delta FEV1, -27.7 ± 2.9%; p = 0.0001). During hyperventilation, the volume of NO rose in both groups. The asthmatic subjects, however, generated approximately 55% more NO/ min than did the normal control subjects even though their level of ventilation was approximately 66% less. In contrast to the normal subjects, NO production in the asthmatics continued into the recovery period after the challenge stopped and FENO rose temporally as the airflow limitation developed. These results suggest that NO plays an intimate role in the development of airway obstruction that follows hyperpnea.




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