A unified diffusion-reaction framework for gas exchange shaped the interpretation of acute lung injury during this period. Research emphasized linking tissue diffusion, alveolar membrane diffusion, reaction kinetics at the capillary interface, and pulmonary blood volume to overall oxygen transfer. Edema was understood as the product of hydrostatic pressure and reduced plasma oncotic pressure, with hypoxia-induced capillary leak and high-altitude edema illustrating permeability- and injury-driven phenotypes that refined ALI pathophysiology.