Arterial Cord Blood Hypoxanthine: A Measure of Intrauterine Hypoxia?

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Abstract
In order to evaluate the concentration of hypoxanthine in the cord blood as an indicator of intrauterine hypoxia, hypoxanthine was determined in the arterial and venous cord blood of 49 randomly chosen newborns and in the peripheral venous blood of their mothers. In addition, 5 young, nonpregnant women were investigated. Term babies with signs of probable intrauterine hypoxia (fetal distress, scalp blood or arterial cord blood pH < 7.19, and/or Apgar score of < 5 at 1 min) had hypoxanthine levels (19.8 ± 3.5 μmol/l) consistently above the mean for normals. However, there was a large variability of hypoxanthine values in normal babies (16.1 ± 5.7 μmol/l) and in those with isolated signs of fetal distress (14.6 ± 6.9 μmol/l). There was no general correlation between the levels of hypoxanthine in arterial cord blood and arterial cord blood pH (r = -0.15) or between the levels of hypoxanthine in arterial cord blood and the Apgar score at 1 min (r = -0.05). At delivery, all mothers had higher levels of hypoxanthine than nonpregnant women (16.0 ± 6.8 vs. 7.6 ± 2.1 μmol/l; p < 0.001). The maternal hypoxanthine values correlated closely with those of the venous cord blood (r = 0.72; p < 0.001). Positive arterio-venous differences in the cord blood increased with progressively higher levels of hypoxanthine in arterial cord blood (r = 0.53; p < 0.001), indicating a clearance through the placenta. The frequently observed negative arterio-venous difference (37 % of all cases) indicates a passage of hypoxanthine from the mother to the baby as well. We conclude: (1) high levels of hypoxanthine in the cord blood probably depend only in part on hypoxia; (2) hypoxanthine equilibrates bidirectionally across the placenta. Therefore, the levels of hypoxanthine found in neonatal cord blood do not provide reliable evidence of intrauterine hypoxia.