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EMISSION PARTICLE-INDUCED VENTILATORY ABNORMALITIES IN A RAT MODEL OF PULMONARY HYPERTENSION
Citation:
Gardner, S. Y., J K. McGee, U P. Kodavanti, A. D. Ledbetter, J. I. EVERITT, D. W. Winsett, D L. Doerfler, AND D L. Costa. EMISSION PARTICLE-INDUCED VENTILATORY ABNORMALITIES IN A RAT MODEL OF PULMONARY HYPERTENSION. ENVIRONMENTAL HEALTH PERSPECTIVES. National Institute of Environmental Health Sciences (NIEHS), Research Triangle Park, NC, 112(8):872-878, (2004).
Impact/Purpose:
To examine the effects of residual oil fly ash on ventilatory function in as a potential contributor to mortality
Description:
Abstract
Preexistent cardiopulmonary disease in humans appears to enhance susceptibility to the adverse effects of ambient particulate matter. Previous studies in this laboratory have demonstrated enhanced inflammation and mortality after intratracheal instillation (IT) and inhalation (INH) of a model emission particles, residual oil fly ash (ROFA), in a rat model of pulmonary vasculitis and hypertension induced by monocrotaline (MCT). The present study was conducted to examine the effects of ROFA in this model on ventilatory function in unanesthetized, unrestrained animals as a potential contributor to the mortality observed. Sixty-day-old male CD rats were injected with MCT (60 mg/kg) or vehicle intraperitoneally 10 days prior to IT ROFA (8.3 mg/kg) or saline (SAL - control) or nose-only INH of ROFA [15 mg/m3 for 6 hours on 3 consecutive days or air (control)]. These ROFA exposures were selected as doses that had previously been shown to exacerbate MCT toxicity. At 24 and 72 hours after exposure, rats were studied individually in a simultaneous gas uptake/whole body plethysmograph. Lungs were removed at 72 hours for histology. Pulmonary test results showed that tidal volume (VT) was decreased 24 hours after IT ROFA in MCT-treated rats. Breathing frequency (f), minute volume (VE), and the ventilatory equivalent for O2 was increased in MCT and vehicle-treated rats 24 hours after IT or INH ROFA and remained elevated 72 hours post-IT. O2 uptake (VO2) also decreased after IT ROFA in MCT-treated rats as did CO uptake at 24 hours, the latter returning to control values in vehicle-treated rats, but remaining low in MCT-treated rats at 72 hours. While ROFA exposure induced histological changes and abnormalities in several ventilatory parameters, many of which were enhanced by MCT treatment, these changes alone did not appear to be life threatening.