Am. J. Respir. Crit. Care Med., Vol 149, No. 1, 01 1994, 220-226.
Smoke inhalation with a concurrent systemic stress results in lung alveolar injury
SR Thom, I Mendiguren, T Van Winkle, D Fisher and AB Fisher
Institute for Environmental Medicine, University of Pennsylvania, Philadelphia 19104-6068.
Smoke inhalation causes injuries to lung airways, and, at times, alveolar
inflammation also develops over approximately 24 h. The pathophysiology of
parenchymal lung injuries is unknown, and it is often fatal. We
hypothesized that an inflammatory stress remote from the smoke-related lung
insult was required for development of alveolar injuries. Spontaneously
breathing rats were exposed, head only, to smoke generated by nonflaming
pyrolysis (smoldering) of Douglas fir wood (DF), polyvinylchloride (PVC),
or the combination of DF+PVC. Intraperitoneal injection of sterile oyster
shell glycogen 4 h before smoke inhalation was used as an extra
inflammatory stimulus. Histologic examinations revealed extensive airway
inflammation in all smoke- exposed groups. Glycogen peritonitis alone
caused no lung injuries, and in the absence of glycogen, smoke inhalation
caused neither parenchymal lung injuries, assessed by [125I]bovine serum
albumin (BSA) leakage, nor neutrophil infiltration, quantified by
myeloperoxidase (MPO) activity. However, in rats pretreated with glycogen
and studied 24 h after exposure to smoke from burning DF+PVC, [125I]BSA
permeability was increased by 232 +/- 41% (SE; n = 13), MPO activity was
increased 5- fold, from 2.6 +/- 0.4 (n = 7) to 13.9 +/- 1.4 (n = 19)
A460/min/g lung, and histopathologic findings included extensive pulmonary
inflammation. We conclude that inhalation of certain types of smoke will
trigger pulmonary injury when an inflammatory process remote from the lungs
is present.
