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METHODS RESPIRATORY COMPLICATIONS are the major source of death from fires today (6, 18, 19, 21, 22, 26, 28, 33, 37). Acute lung damage can occur due to smoke inhalation alone without surface burns (2, 3, 33), and it is the chemical toxins in smoke, not the heat, that produces the injury (13). Smoke delivered to animals will produce a delayed-onset noncardiogenic pulmonary edema, as is frequently seen clinically in human fire victims (2, 33, 37). The composition of smoke is complex and varies widely depending on the material burned and at what temperature. To sort out effects of specific smoke components, we sought to investigate the pulmonary response in dogs to a synthetic smoke consisting only of carbon particles (l-7.5 pm diam), heated air, and an individual selected toxin. Carbon was used as a carrier for the toxin to condense on, since toxin droplets alone may settle out in larger airways or may be exhaled, depending on droplet size. HCl was chosen as the initial 0161-7567/M $1.50 Copyright Animal preparation. Twenty-five mongrel dogs weighing from 14.5 to 37.5 kg [27 t 1.5 (SE)] were anesthetized with intravenous pentobarbital sodium (30 mg/kg induction, 10 mg kg-â h-l maintenance),
Journal of Applied Physiology – The American Physiological Society
Published: Mar 1, 1988
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