EFFECT OF REDUCING ALVEOLAR SURFACE-TENSION ON STRESS FAILURE IN PULMONARY CAPILLARIES

We previously showed that when pulmonary capillaries are exposed to hi gh transmural pressures, stress failure of the blood-gas barrier occur s. It has been suggested that the surface tension of the alveolar lini ng layer may protect against stress failure because at high transmural pressures the capillaries bulge into the alveolar spaces. To test thi s hypothesis, we abolished the gas-liquid surface tension of the alveo li by filling rabbit lungs with normal saline. The lungs were then per fused at capillary transmural pressures of 32.5 or 52.5 cmH(2)O for 1 min with autologous blood, the blood was washed out with a saline-dext ran mixture (3 min), and the lungs were fixed for electron microscopy with buffered glutaraldehyde; all perfusions were done at the same pre ssure. The frequency of breaks was measured in the capillary endotheli al layer, alveolar epithelial layer, and basement membranes, and the d ata were compared with those in air-filled lungs at the same capillary transmural pressure and lung volume. We found that the frequency of b reaks in the endothelium was not significantly different between air a nd saline filling and that there were fewer breaks in the outer bounda ry of the epithelial cells. By contrast, after saline filling, a large r number of breaks were seen in the inner boundary of the epithelium. The frequency of disruptions of the inner boundary of the epithelium w as closely correlated with the volume of edema fluid collected at the trachea during the perfusion. These breaks in the inner boundary of th e epithelium had not previously been seen in air-filled lungs exposed to the same pressures. The results suggest that abolishing the surface tension of the alveolar lining layer removes support from parts of th e blood-gas barrier when the capillaries are subjected to a high trans mural pressure but that not all portions of the barrier are subjected to the same forces.