|| Checking for direct PDF access through Ovid
1. Our aim was to identify mechanisms whereby prolonged fetal hypoxaemia alters renal function and urine production in fetal sheep.2. Fetal hypoxaemia was induced for 24 h by reducing uterine blood flow at 129.0 ± 2.1 days of gestation (term 145-147 days), causing a reduction in fetal arterial O2 saturation (SaO2) from 52.5 ± 2.3 to 22.0 ± 1.3% (P < 0.05). This hypoxaemia was initially associated with a mild acidaemia (pH 7.23 ± 0.03).3. The glomerular filtration rate (GFR) increased from a control value of 1.8 ± 0.3 mL/min per kg to a maximal value of 2.8 ± 0.6 mL/min per kg (P < 0.05) at 4-5 h of hypoxaemia, returning to control levels by 6-9 h of hypoxaemia. After 4 h of hypoxaemia renal blood flow was no different to control values (144 ± 8 mL/min per 100 g kidney weight) but after 24 h of hypoxaemia it had increased to 190 ± 8 mL/min per 100 g kidney weight (P < 0.05). Fractional reabsorption of Na+ in the proximal tubules decreased from a control value of 81.5 ± 2.2 to 65.2 ± 3.9% at 2-3 h of hypoxaemia(P < 0.05) and remained reduced (68.5 ± 3.1%) at the end of hypoxaemia (P < 0.05). Fetal mean arterial pressure transiently increased (P < 0.05) but returned to control values by 4-5 h of hypoxaemia. Fetal renal vascular resistance was not significantly altered during hypoxaemia. Fetal urine production increased from a control value of 12.3 ± 2.1 mL/h per kg to a maximal value of 19.1 ± 4.2 mL/h per kg at 4-5 h of hypoxaemia (P < 0.05) and returned to control by 24 h of hypoxaemia.4. Our results indicate that prolonged fetal hypoxaemia leads to the inhibition of Na+ reabsorption in the proximal portion of the renal tubules. Changes in GFR induced by hypoxaemia were similar to those in fetal urine production and were not associated with changes in renal blood flow. We conclude that prolonged fetal hypoxaemia affects renal haemodynamics and the reabsorptive capacity of the renal tubules, resulting in a diuresis.