Morphologic changes in pulmonary oxygen toxicity

JD Crapo - Annual review of physiology, 1986 - annualreviews.org
Annual review of physiology, 1986annualreviews.org
Exposure to high concentrations of oxygen has been demonstrated to cause alterations
throughout the respiratory tract in humans and other animals. Changes occur in the airway
epithelium, the arterial vascular bed, the alveolar septa, and in the pleural space.
Atelectasis, interstitial and alveolar edema, pleural effusions, and changes in cell function
and structure occur. The morphologic changes that occur in the lung in response to
inhalation of high concentrations of oxygen were first described in 1897-1899 by J. Lorraine …
Exposure to high concentrations of oxygen has been demonstrated to cause alterations throughout the respiratory tract in humans and other animals. Changes occur in the airway epithelium, the arterial vascular bed, the alveolar septa, and in the pleural space. Atelectasis, interstitial and alveolar edema, pleural effusions, and changes in cell function and structure occur. The morphologic changes that occur in the lung in response to inhalation of high concentrations of oxygen were first described in 1897-1899 by J. Lorraine Smith (24, 25) who characterized the acute histologic features as including atelectasis, inflammation, and vascular congestion, with death due to con solidation of the lungs from congestion and exudation into the alveoli. This has subsequently been defined as the early or exudative phase of severe pulmonary oxygen toxicity. Multiple investigators have confirmed similar morphologic patterns in a wide variety of animal species (6), including primates (19) and man (14, 18, 22).
Among the most dramatic effects are those involving the cells of the alveolar septum. Kistler et al (20) used electron microscopy to identify qualitatively and quantitatively many of the changes occurring in rat lungs. The earliest change was a twofold increase in the width of the interstitial space caused initially by edema. Subsequently the number of interstitial cells and interstitial matrix elements increased. The capillary endothelial cell was identified as one of the primary targets of oxygen-mediated cell injury; cytoplasmic changes in these endothelial cells were followed by fragmentation and cell destruction. These changes in the lung microvasculature are those most closely associated with events leading to death of animals given lethal doses of hyperoxia.
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