AJP - Lung Cellular and Molecular Physiology, Vol 267, Issue 6 797-L806, Copyright © 1994 by American Physiological Society
Progressive alveolar septal injury in primates exposed to 60% oxygen for 14 days
J. D. Crapo, G. Hayatdavoudi, M. J. Knapp, P. J. Fracica, W. G. Wolfe and C. A. Piantadosi
Department of Medicine, Duke University Medical Center, Durham, North Carolina 27710.
Moderate exposures to hyperoxia are becoming increasingly common in
clinical medicine as advancing technology allows O2 to be more effectively
delivered to nonintubated patients. The sensitivity of the lung to injury
by a subchronic exposure to 60% O2 was investigated, using baboons and
serial lobar biopsies. Because results obtained from different regions of
the lung were compared, the alveolar architecture of different lung lobes
of three controls was studied, with the use of electron microscopic
morphometric analyses, to assess possible lobar differences in volume,
surface, and numerical densities of cells and tissues. In animals exposed
to 60% O2, the same techniques were used to assess specific tissue changes
in the epithelial, interstitial, and endothelial compartments of the
alveolar septa. All six lobes of the normal baboon lung were found to be
identical with respect to alveolar architecture. Thus, for gases of low
reactivity and given in high concentrations, such as O2, cross-comparisons
between different lobes are appropriate. Exposure to 60% O2 was found to
cause proliferation of alveolar type II epithelium, suggesting a low-grade,
chronic epithelial injury. Animals allowed to recover for 8 wk in room air
showed progressive changes in the alveolar interstitium, involving
increases in both cells and matrix. Because sequential lobar resections
were done, animals were exposed both to 60% O2 and to the effects of
general anesthesia and thoracotomies. The exposure to 60% O2 for 2 wk in
this experimental setting leads to an alveolar septal injury that includes
a progressive interstitial fibrotic response.
