The Science Journal of the American Association for Respiratory Care

2007 OPEN FORUM Abstracts

DISTURBANCE OF BREATHING AND PULMONARY INJURY AFTER BRIEF INHALATION OF HIGH LEVEL NITROGEN DIOXIDE IN AWAKE RATS

Z. Gu1, A. J. Januszkiewicz1, T. J. Atkin1, V. I. Morthole1, G. D. Coleman1


Background: Nitrogen dioxide (NO2) could be released to the environment from burning nitrogenous materials in fire, or explosions of military munitions, even a detonation of terrorist devices. Our understanding of pulmonary function after exposure to high levels of NO2 is limited. It is important to clarify the pulmonary injuries in order to better develop the strategies in respiratory care for patients suffered from high level NO2 exposure.

Method: Male Sprague-Dawley rats were placed into restrainers of an exposure chamber and breathed medical-grade air for5 minutes prior to exposure. Animals were then continuously exposed to NO2 for 5 minutes. Concentrations of NO2 were monitored by a dual-bean IR-UV spectrophotometer. Respiratory data were collected and analyzed using CODAS system. Respiratory changes were represented by percent of the baseline. Lung wet-to- dry ratio was measured. Lung tissues were fixed using formaldehyde and routine-pathologically processed. Statistical comparisons were conducted using analysis of variance (ANOVA).

Results: 1) During a 5-minutes exposure to NO2, minute ventilation volume (VE) and breathing rate (BR), were quickly dropped at the first minute and sustained in entire period of the exposure. In the 500, 1000, and 2000 ppm NO2 groups the responses to NO2 inhalation were dose-dependent. VE in the 2000 ppm group decreased to 38% of its baseline. 2) At 24 hrs after exposure, VE and BR were recovered in 500 and 1000 ppm groups. But they did not recover in 2000 ppm group. VE in the 2000 ppm group was 72% of its baseline. 3) Lung wet-to-dry ratio showed no change in 500 ppm group. Slight increase of lung wet-to-dry ratio showed in 1000 ppm group. Significant increase of wet-to-dry ratio occurred in the 2000 ppm group. 4) At 24 hrs after exposure, the lungs in 500 and 1000 ppm groups did not show significant histo-pathological changes. However, lung edema was found in 2000 ppm group.

Conclusions: 1) Acute respiratory disturbance caused by a 5-minute exposure to NO2 at concentrations lower than 1000 ppm could be recovered within 24 hrs. However, pulmonary disorders caused by exposure to NO2 at the level as high as 2000 ppm could develop a delayed lung injury showing lung edema within 24 hrs and characterized by lower minute ventilation volume. 2) These data provide dynamic information about acute effects of NO2 on respiratory pattern and fill data-gaps necessary to make strategies in the management of respiratory care.

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