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Inhaled nitric oxide attenuates bronchoconstriction in canine peripheral airways
D R Gwyn1, K S Lindeman, C A Hirshman
1Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.
American Journal of Respiratory and Critical Care Medicine
|February 1, 1996
Summary
Inhaled nitric oxide (NO) relaxes airway smooth muscle. This study shows NO also dilates peripheral airways, suggesting it may treat lung diseases by relaxing constricted airways.
Area of Science:
- Pulmonary Physiology
- Respiratory Medicine
Background:
- Inhaled nitric oxide (NO) is a vasodilator.
- NO relaxes vascular and airway smooth muscle.
- NO's bronchodilator effects in central airways are known, but effects on peripheral airways are not.
Purpose of the Study:
- To determine if NO directly relaxes peripheral airways.
- To investigate NO's ability to attenuate hypocapnia- and acetylcholine-induced constriction in peripheral airways.
Main Methods:
- Peripheral airway resistance (RP) was measured in anesthetized dogs using a wedged bronchoscope.
- RP was increased by hypocapnia or aerosolized acetylcholine.
- NO was delivered directly to the lung periphery.
Main Results:
- Nitric oxide (14.5 to 250 ppm) attenuated hypocapnia-induced constriction by 38-74%.
- Nitric oxide attenuated acetylcholine-induced constriction by 36-52%.
- These effects were observed with inhaled NO < 100 ppm.
Conclusions:
- Inhaled nitric oxide acts as a bronchodilator in the lung periphery.
- NO may treat lung diseases by relaxing airway and/or vascular smooth muscle.