Inhibition of active sodium absorption leads to a net liquid secretion into in vivo rabbit lung at two levels of alveolar hypoxia.

Active sodium transport across alveolar epithelium is known to contribute to the resolution of pulmonary oedema. We have attempted to assess whether sodium transport is essential to prevent liquid accumulation in healthy pulmonary alveoli exposed to mild hypoxia, and whether its contribution to liquid absorption differs between mild and moderate levels of hypoxia. In twenty-four anaesthetized adult rabbits we used direct bronchial cannulation to measure liquid movement from the liquid-filled left lung over 3.5 h. Half of the rabbits were studied at a level of mixed venous (and alveolar) oxygen partial pressure, PVO2, of 6.5 kPa and half at 4.5 kPa. PVO2 was altered by changing the inspired oxygen fraction in the ventilated right lung. Alveolar hydrostatic pressure was 0.3 kPa. In each group of 12, six animals with inhibitors of sodium transport in the isosmotic instillate were compared with six controls. We have shown an alveolar liquid secretion (approximately 0.6 microl min(-1) (kg body weight)(-1)) in the presence of inhibitors of active transport and an absorption (approximately 4 microl min(-1) (kg body weight)(-1)) in controls. Changing PVO2 had no influence on these movements. We conclude that, in this model of pulmonary oedema, active sodium transport appears to be essential for prevention of alveolar liquid accumulation via secretion. Furthermore, the contribution of active sodium transport to liquid absorption remains constant at oxygen tensions between 4.5 and 6.5 kPa.