Inhibition of nitric oxide synthesis attenuates thermally induced asthma.
Kotaru, C., M. Skowronski, A. Coreno, and E. R. McFadden, Jr.
Airway Disease Center, Division of Pulmonary and Critical Care Medicine,
University Hospitals of Cleveland, and Department of Medicine, Case Western Reserve
University School of Medicine, Cleveland Ohio 44106
APStracts 8:0250A, 2001.
To determine whether the inhibition of nitric oxide (NO) synthesis attenuates thermally
induced obstruction, we had 10 asthmatic volunteers perform isocapnic hyperventilation
with frigid air after inhaling 1 mg of NG-monomethyl-l-arginine (l-NMMA) or isotonic
saline in a blinded fashion. The challenges were identical in all respects, and there were
no differences in baseline lung function [1-s forced expiratory volume (FEV1); saline 2.8
± 0.3 liters, l-NMMA 2.9 ± 0.3 liters; P = 0.41] or prechallenge fractional concentration
of nitric oxide in the exhaled air (FeNO) [saline 23 ± 6 parts/billion (ppb), l-NMMA 18 ±
4 ppb; P = 0.51]. Neither treatment had any impact on the FEV1, pulse, or blood
pressure. After l-NMMA, FeNO fell significantly (P < 0.0001), the stimulus-response
curves shifted to the right, and the minute ventilation required to reduce the FEV1 20%
rose 53.5% over control (P = 0.02). The results of this study demonstrate that NO
generated from the airways of asthmatic individuals may play an important role in the
pathogenesis of thermally induced asthma.
Received 31 October 2000; accepted in final form 16 April 2001
APS Manuscript Number A1063-0.
Article publication pending J Appl Physiol
ISSN 1080-4757 Copyright 2001 The American Physiological Society.
Published in APStracts on 18 June 2001