A murine model of smoke inhalation

Citation
E. Matthew et al., A murine model of smoke inhalation, AM J P-LUNG, 280(4), 2001, pp. L716-L723
Citations number
33
Categorie Soggetti
da verificare
Journal title
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
ISSN journal
10400605 → ACNP
Volume
280
Issue
4
Year of publication
2001
Pages
L716 - L723
Database
ISI
SICI code
1040-0605(200104)280:4<L716:AMMOSI>2.0.ZU;2-4
Abstract
The United States has one of the world's largest per capita fire death rate s. House fires alone kill >9,000 Americans annually, and smoke inhalation i s the leading cause of mortality from structural fires. Animal models are n eeded to develop therapies to combat this problem. We have developed a muri ne model of smoke inhalation through the design, construction, and use of a controlled-environment smoke chamber. There is a direct relationship betwe en the quantity of wood combusted and mortality in mice. As with human vict ims, 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 e xposed to wood smoke demonstrated more dramatic pathology than mice exposed to cotton or polyurethane smoke. A CD-1 model of wood smoke exposure was d eveloped, demonstrating type II cell hypertrophy, cytoplasmic blebbing, cyt oplasmic vacuolization, sloughing, hemorrhage, edema, macrophage infiltrati on, and lymphocyte infiltration. The bronchoalveolar lavage fluid of smoke- exposed mice demonstrated a significant increase in total cell counts compa red with those in control mice. These findings are comparable to the lung t issue response observed in human victims of smoke inhalation.