ABSTRACT
Acute alveolar injury (AAI) was strictly defined and judged to be the major cause of respiratory failure. In the cases associated with pulmonary infections AAI coexisted with and clearly affected many areas of lung not involved by the infectious lesion. Because AAI is defined morphologically, a clear understanding of its structural evolution is critical in evaluating the relevance of any experimental model to the condition seen in humans. Hyperoxic injury is caused, at least principally, by toxic oxidant radicals apparently generated by two closely interrelated mechanisms. The initial phase of hyperoxic injury occurs because lung cells exposed to increased oxygen tension produce toxic oxygen radicals in excess of the ability of the cells antioxidant enzymes to quench them. The morphologic changes in the lung after exposure to hyperoxia vary with the species and age of the animal, the concentration of inspired oxygen, and the duration of exposure.
