Renal acid-base and sodium handling in hypoxia and subsequent mild metabolic acidosis in foetal sheep

1. To measure the renal contribution to acid-base homeostasis during hypoxi a (not associated with hypercapnia) and in response to the subsequent mild metabolic acidosis and to determine the effects of this hypoxia on the rena l handling of sodium, studies were performed in six chronically catheterize d foetal sheep (129-138 days gestation) before, during and for Ih after a 2 h period of hypoxia. 2. Hypoxia was induced in the conscious ewe by infusing nitrogen into the t rachea. Foetal arterial oxygen tension fell to 12.0+/-0.6 mmHg (P < 0.001). Carbon dioxide tension fell during hypoxia (P < 0.001) and was still somew hat reduced in the recovery period (P < 0.005). Arterial pH fell progressiv ely to 7.19+/-0.08 in the recovery period (P < 0.05). Plasma bicarbonate co ncentrations fell (P < 0.001) and lactate rose (P < 0.001). 3. Urinary pH and the excretion rates of bicarbonate, titratable acid, ammo nium and net acid did not change during hypoxia, Ammonium excretion and, he nce, generation of new bicarbonate increased in the recovery period (P < 0. 05). 4. Renal sodium excretion progressively increased and was greatest after no rmoxia was restored (P < 0.05). This natriuresis was due to a fall in the r eabsorption of sodium by the proximal tubule (P < 0.05). Proximal reabsorpt ion of sodium was directly related to foetal pH (P < 0.0001) and bicarbonat e reabsorption (P < 0.001). 5. It was concluded that: (i) the foetal kidneys began to contribute to the maintenance of acid-base balance within the first hour of recovery from a 2 h episode of hypocapnic hypoxia, even though the acidosis was relatively mild; and (ii) a reduction in bicarbonate reabsorption was probably the mos t important factor that limited sodium reabsorption by the renal tubule dur ing this experiment.