A series of 29 newborn infants had been studied after intrapartum hypoxia defined as meconium aspiration, an Apgar score of less than or equal to 6 at 5 min or a peripheral blood pH of 7.2 or less after resuscitation. Two independent sets of techniques were used; one concerned with the critical system in hypoxic damage, the central nervous system, the other assessing the central biochemical events in hypoxia. Both sets of data were assembled, then graded separately and only then combined. In this way detailed neurological assessment has been combined with measurement of urinary excretion of the ATP metabolites, hypoxanthine and xanthine. The essential metabolic consequence of hypoxia is a reduction in the synthesis of the energy currency of cells, ATP. This is associated with an outflow of ATP metabolites from cells. The extent of neurological damage was related to the magnitude of the hypoxanthine and xanthine excretion; neither were closely related to the initial blood pH. Infants who were normal neurologically had normal oxypurine excretion. Infants with neurological abnormalities for less than 48 h had lower excretion than those who were abnormal for more than 48 h. The duration of abnormal oxypurine excretion after an acute episode of hypoxia was studied in two infants with respiratory distress and in two other infants with apnoeic attacks. Severe hypoxia was followed by abnormal oxypurine excretion for at least 40 h after an acute episode. It is justifiable to suggest that abnormalities of oxypurine excretion should indicate intrapartum hypoxia in newborn infants. This excretion should also quantify the metabolic damage.
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