The pathogenesis of reexpansion pulmonary edema has not been well studied. We tested the hypothesis that both long term collapse and subsequent reexpansion of the lungs cause reexpansion pulmonary edema by increasing pulmonary microvascular permeability. We investigated lymph dynamics in 15 experiments on collapsed lung and 10 experiments after lung reexpansion in 14 unanesthetized sheep with chronic lymph fistulas. We found that 24-hr left lung collapse increased lymph flow through the caudal mediastinal lymph node from the baseline of 1.71 +/- 0.97 (mean +/- S.D.) g/15 min to 2.01 +/- 0.99 g/15 min, although 2-hr collapse did not affect lymph flow. The L/P ratio did not fall below baseline in either experiment. Pulmonary arterial pressure increased by only about 6 cmH2O both in 2-hr and 24-hr collapse. Reexpansion after 24-hr lung collapse also increased lymph flow from the baseline of 1.64 +/- 0.52 g/15 min to 3.20 +/- 0.79 g/15 min during the first 2 hr after reexpansion. The lymph-to-plasma protein concentration ratio did not fall below the baseline. Reexpansion after 2-hr collapse did not affect these variables. We conclude that both long term lung collapse and subsequent reexpansion lead to reexpansion pulmonary edema by increasing pulmonary microvascular permeability.