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 t o the resolution of pulmonary oedema. We have attempted to assess whether s odium transport is essential to prevent liquid accumulation in healthy pulm onary alveoli exposed to mild hypoxia, and whether its contribution to liqu id absorption differs between mild and moderate levels of hypoxia. In twent y-four anaesthetized adult rabbits we used direct bronchial cannulation to measure liquid movement from the liquid-filled left lung over 3.5 h. Half o f the rabbits were studied at a level of mixed venous (and alveolar) oxygen partial pressure, P (v) over bar (O 2), of 6.5 kPa and half at 4.5 kPa. P (v) over bar (O 2) was altered by changing the inspired oxygen fraction in the ventilated right lung. Alveolar hydrostatic pressure was 0.3 kPa. In ea ch group of 12, six animals with inhibitors of sodium transport in the isos motic instillate were compared with six controls. We have shown an alveolar liquid secretion (approximately 0.6 mul min(-1) (kg body weight)(-1)) in t he presence of inhibitors of active transport and an absorption (approximat ely 4 mul min(-1) (kg body weight)(-1)) in controls. Changing P (v) over ba r (O 2) had no influence on these movements. We conclude that, in this mode l 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 consta nt at oxygen tensions between 4.5 and 6.5 kPa.