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Sulfur mustard inhalation induced respiratory lesions in guinea pigs: Physiological, biochemical, and histological study

TitleSulfur mustard inhalation induced respiratory lesions in guinea pigs: Physiological, biochemical, and histological study
Publication TypeReport
Year of Publication1993
AuthorsAllon N., Gilat E., Amir A., Fishbeine E., Liani H.
Series TitlePentagon Reports
Pagination8
InstitutionArmy Medical Research Institute of Chemical Defense
CityAberdeen Proving Ground, MD
ISBN NumberP667800
KeywordsADDITION, ALVEOLI, Animals, BRONCHI, DAMAGE, DEHYDROGENASESZ, DEHYDROGENASESZRESPIRATORY SYSTEM, DIFFUSION, ENZYMES, EXPOSURE(PHYSIOLOGY), FLUIDS, GLUTATHIONE, Guinea Pigs, HISTOPATHOLOGY, INHALATION, INTERVALS, LACTIC DEHYDROGENASE, LESIONS, LUNG, MODELS, MUSTARD AGENTS, PARAMETERS, PROTEINS, RATES, RECOVERY, REDUCTION, RESPIRATORY SYSTEM, Sulfur, TIME, TIME INTERVALS, TOXICITY, TRACHEA, VAPORS, VOLUME
Abstract

Inhalation exposure to sulfur mustard (SM) vapor causes long term damage to the respiratory system. The lesions were characterized by specific physiological, biochemical and histopathological methods. Awake 128 guinea-pigs (GP) were exposed for 10 min to SM (1200-1700 microns x min/1). Respiratory parameters were monitored per animal before, during and after the exposure using plethysmograph's. Biochemical and histological evaluations were performed at different time intervals for up to 7 days post exposure. SM inhalation resulted in a decrease in both respiratory rate and minute volume, and in an increase in tidal volume. These changes occurred immediately after the onset of exposure and lasted for up to 7 days. The changes in the respiratory parameters were accompanied by a massive reduction in O2 diffusion capacity. Evaluation of bronchoalveolar lavage (BAL) fluid, indicated neutrophil infiltration, an increase in the protein content, and in the activity of both lysosomal enzymes and lactic dehydrogenase (LDH) in the alveolar space. In addition, a decrease in glutathione content was observed one day post exposure in the BAL fluid and the lung whereas an increase in lung glutathione content was observed 6 days later. Histological evaluation of the lungs and trachea revealed severe lesions in both tissues. Recovery was incomplete 7 days post exposure. The detailed characterization of the effect of SM inhalation offers a reliable model for the evaluation of potential therapies against SM exposure.

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