The influx of leukocytes into the lung during hyperoxic exposures has been suggested as a significant contributor to alveolar injury because, when activated, they can cause damage by producing oxygen radicals and releasing hydrolytic enzymes. To better understand the relationship between hyperoxic injury and inflammatory responses, morphometric methods were used to quantitate changes in alveolar capillary blood components of rats exposed to 100% and 85% oxygen. After 40 h in 100% oxygen the absolute volume of platelets in the capillary bed increased 78% and there was a 111% increase in the total endothelial cell surface area covered by platelets. There were no significant changes in these parameters for neutrophils until 60 h of exposure of 100% O2. At this point, both the absolute volume and the endothelial surface area covered by neutrophils increased more than threefold. After 3 days in 85% oxygen absolute platelet volume was almost doubled and the surface area covered by platelets increased 79%. No neutrophil increases occurred until 5 days exposure to 85% oxygen, and both absolute volume and surface area dropped to less than control values after 7 days of exposure. The appearance of platelets prior to an influx of neutrophils during both hyperoxic exposures suggests that the initial endothelial cell injury results from an increased intracellular production of oxygen radicals rather than being due to oxygen radicals produced by leukocytes. Endothelial cell membrane changes were associated with the initiation of platelet accumulation in the capillary bed. Platelet components released during platelet activation may be important mediators for the subsequent neutrophil influxes.(ABSTRACT TRUNCATED AT 250 WORDS)