Since hypoxia is associated with sympathetic activation, we hypothesized that the course of hypoxic lung injury might bear some resemblance to that induced by stimulation with catecholamines (CA). Therefore, we compared the features of hypoxic lung injury with those previously observed after CA infusion. Rats were exposed to normobaric hypoxia over time intervals from 6 to 168 h. Animals kept under normoxic conditions served as controls. After heart catheterization, lung tissue was obtained for histology and analysis of mRNA expression of cytokines and extracellular matrix (ECM) molecules. In contrast to CA stimulation, significant hemodynamic changes such as increase in total peripheral resistance occurred as late as after 168 h of hypoxic exposure. Moderate pulmonary edema appeared after 8h and peaked after 16h of hypoxic exposure. It was accompanied by inflammation, fibrosis and vascular hypertrophy. After 3 days of hypoxia, mRNA expression of collagen type I and III and of other ECM molecules was significantly increased. The results demonstrate a similar time course of hypoxic and CA-induced pulmonary injuries. However, differential temporal relations between hemodynamic changes and edema formation indicate a different role of hemodynamic factors in the two models of pulmonary injury.