“…(20 , 27), hyperplasia of alveolar Type II cells ( 1,20) , accumula tion of in ters titial and alveolar fluid (6 , 16) , depos ition of hyaline membranes (6 , 41), and in terference with the forma tion or func tion of pulmonary surfactant (11). Physiological manifestations of these changes result in decreasing 02 uptake because of impaired diffusion (5,18), V/~ abnormalities ( 6 ), decreased pulmonary compliance ( 5 ), and alveolar atelectasis ( 6,35). Desp ite this rather detailed description of the morphological and physiological changes resultant from the chronic inhalation of oxygen , the biochemical bases of these lesions are ouly speculative.…”