Abstract
When exposed to hyperoxia, patients and animals develop significant lung injury which may lead to respiratory failure and even death. Changes seen in lungs exposed to hyperoxia indicate that endothelial cell damage with vascular leak is a prominent and early feature of the pathophysiology of pulmonary oxygen toxicity. We hypothesized that hyperoxia directly damages endothelial cells, leading to vascular leak and compromise of gas exchange. To test this hypothesis, we exposed monolayers of bovine pulmonary artery endothelial cells to hyperoxia (95% O2 - 5% CO2) or normoxia (80% N2 - 15% O2 - 5% CO2) at ambient atmospheric pressure for 24, 48, 72 and 96 hours. We found that exposure to hyperoxia caused increasingly severe morphologic changes in endothelial cells, manifested by clumping of nuclear material and gross cytoplasmic disorganization. Such changes appeared in increasing proportions of cells between 24 and 96 hours of hyperoxic exposure, but were rarely seen in cells exposed to normoxia. These changes are quite similar to those found in the lung endothelial cells of animals exposed to hyperoxia. We also found increasing release of cytoplasmic lactic dehydrogenase from the hyperoxia-exposed but not normoxia-exposed cells. These results suggest that hyperoxia alone can damage pulmonary endothelial cells and support the possibility that this mechanism may contribute to the respiratory failure seen in oxygen toxicity.
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Bowman, M., Harada, R., Delong, S. et al. 1632 HYPEROXIA DAMAGES ENDOTHELIAL CELLS IN TISSUE CULTURE. Pediatr Res 15 (Suppl 4), 715 (1981). https://doi.org/10.1203/00006450-198104001-01649
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DOI: https://doi.org/10.1203/00006450-198104001-01649