Chronic heart failure (CHF) is associated with adaptive structural changes at the alveolocapillary barrier, which may be associated with altered protein permeability. Bi-directional protein movement across the barrier was studied in anesthetized rats with infarct-induced CHF by following ¹²⁵ I-albumin flux into the alveoli and, the leakage of surfactant protein-B (SP-B) from the alveoli into the circulation. Three groups were studied: controls (0% left ventricular infarct), moderate infarct (25-45%) and large infarct (>46%). Wet and dry-lung weights increased in the large infarct group (both p<0.001), consistent with increased lung water and solid lung tissue. ¹²⁵ I-albumin flux increased across the endothelial (p<0.001) and epithelial (p<0.01) components of the alveolocapillary barrier in the large infarct group. Plasma SP-B increased 23% with moderate infarcts (p<0.05) and 97% with large infarcts (p<0.001), independent of alveolar levels. Lavage fluid immune cells (p<0.01), and myeloperoxidase activity (p<0.05) increased in the large infarct group, consistent with inflammation. Bi-directional protein movement across the alveolocapillary barrier is increased in CHF, and alveolar inflammation may contribute to this pathophysiological defect.