SummaryThe measurement of arterial plasma concentration of hypoxanthine in 16 healthy newborn infants showed a prominent increase after birth compared with the umbilical cord levels. Peak values were found 10-20 min after birth with a maximal value of 11.9 pmole/liter in the normal newborns. In five asphyxiated infants the postnatal pattern of hypoxanthine was the same as for normal infants but the increase was even more prominent. A mean peak value of 33.7 pmole/liter was noted in the asphyxiated infants. Our results indicate that the hypoxanthine concentration is influenced not only by the degree of hypoxia, but also by the peripheral circulation and the time interval between the hypoxic event and the blood sampling. It is concluded that hypoxanthine assay may be of clinical value for the detection of past hypoxia as a semiquantitative test.
SpeculationIt is possible to differentiate a group of asphyxiated infants from normal infants by measurements of plasma hypoxanthine concentration. A new biochemical measure of perinatal hypoxia thus appears available. Knowledge about the change in hypoxanthine concentration is however of much greater value than that of a single plasma sample which may be &isleading.The theoretical connection between lack of oxygen, reduced cellular energy contents, and the catabolism of energy-rich phosphates (e.g., ATP, ADP) has been known for a long time. Until recently, however, the estimation of purine metabolites has not been used in clinical practice as a measure of hypoxia. With a micromethod for determination of the hypoxanthine concentration in plasma, Saugstad (18) found this metabolite to be a sensitive sign of hypoxia in experimental animals (20,21,22,23,24) and his preliminary clinical results also indicated a constant and slow decrease of this concentration after a period of fetal hypoxia. He therefore proposed that hypoxanthine measurements could be used for a retrograde estimation of past episodes of hypoxia in the newborn infant (19). In the umbilical cord plasma a hypoxanthine level of 11 pmole/liter was found to discriminate newborn infants with normal deliveries from infants with signs of intrauterine asphyxia (19). Lipp et al. (1 l), however, found that the hypoxanthine concentration in umbilical cord plasma from asphyxiated newborn infants overlapped in a rather broad range the values obtained from normal infants. This was true for both arterial and venous cord blood.In view of this discrepancy, the present study was undertaken in order to investigate the change in postnatal arterial hypoxanthine concentration in a number of normal and asphyxiated newborn infants who had been carefully monitored during delivery and in the early postnatal period. In some of these infants, the hypoxanthine concentration was also measured in venous cord blood and in the immediate neonatal period in blood samples obtained from the umbilical vein.