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Am J Physiol Lung Cell Mol Physiol 2001 Apr;280(4):L716-23

A murine model of smoke inhalation.

Matthew E, Warden G, Dedman J.

Department of Molecular and Cellular Physiology, University of Cincinnati
Medical Center, 231 Bethesda Ave., Cinncinnati, OH 45267-0576, USA.

The United States has one of the world's largest per capita fire death rates.
House fires alone kill >9,000 Americans annually, and smoke inhalation is the
leading cause of mortality from structural fires. Animal models are needed to
develop therapies to combat this problem. We have developed a murine model of
smoke inhalation through the design, construction, and use of a
controlled-environment smoke chamber. There is a direct relationship between the
quantity of wood combusted and mortality in mice. As with human victims, the
primary cause of death from smoke inhalation is an elevated blood
carboxyhemoglobin level. Lethal (78%) and sublethal (50%) carboxyhemoglobin
levels were obtained in mice subjected to varying amounts of smoke. Mice exposed
to wood smoke demonstrated more dramatic pathology than mice exposed to cotton
or polyurethane smoke. A CD-1 model of wood smoke exposure was developed,
demonstrating type II cell hypertrophy, cytoplasmic blebbing, cytoplasmic
vacuolization, sloughing, hemorrhage, edema, macrophage infiltration, and
lymphocyte infiltration. The bronchoalveolar lavage fluid of smoke-exposed mice
demonstrated a significant increase in total cell counts compared with those in
control mice. These findings are comparable to the lung tissue response observed
in human victims of smoke inhalation.

PMID: 11238012 [PubMed - indexed for MEDLINE]

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