A previous study of hamsters, 21 days after intratracheal treatment with pancreatic elastase, showed development of emphysema, shift of the volume-pressure curve up an to the left, with both air and saline filling, and increase in quasistatic lung compliance. There was also a striking increase in vital capacity and lung volume at transpulmonary pressure of 25 cm H2O (TLC25); however, 21 days after collagenase treatment, there was only a slight increase in TLC25. The lung volume changes were not consistent with the theory that the collagen fiber network is responsible for limiting distension of the lung. This report considers saline-filled volume-pressure curves studied in excised hamster lungs after incubation with endotracheally instilled pancreatic elastase or clostridial collagenase solutions. Fluid retained in the lungs after the first infusion-withdrawal cycle was significantly greater in lungs treated with elastase than in lungs treated with collagenase or in control lungs. Total fluid volume at full inflation was similar in the 3 groups. Chord compliance of lungs treated with collagenase was greater at high volume range than that in lungs treated with elastase or control lungs; chord compliance of elastase-treated lungs was higher at mid-volume range than that of collagenase-treated or control lungs. The results of these in vitro studies are consistent with the theory of independently functioning elastic and collagen fiber networks, with the latter limiting lung distensibility at high volumes, and the former providing great extensibility at low volumes. Events that are part of the repair process after elastase injury may result in a change in the orientation of collagen in alveolar tissue and appear to account for the differing effects of in vivo and in vitro elastase treatment on the static mechanical properties of the lungs.