Abstract
The HX concentration is a specific indicator of tissue hypoxia. The plasma level of this purine metabolite can be used to assess intracellular energy status. Extensive animal studies, but less clinical data haveevaluated monitoring this metabolite in routine clinical work. In the present study plasma HX has been determined according to the micromethod previously described (Saugstad, 1975). Umbilical cord blood from normal delivery & after asphyxia (by Apgar score & cardiotocographic tracings) were studied. The mean HX concentration in non-asphyxiated babies was 9 μmol/1 (±2SD=0-22 μmol/1). In babies with moderate asphyxia, the HX level was elevated (26-40 μmol/1). Arterial plasma HX from neonates with & without tissue hypoxia (by clinical signs & acid-base status) in 18 samples showed linear correlation between plasma HX & base deficit (BD): (BD=0.44HX -1.8 r=0.66 p<0.01). BD ranged between -6 & 21 μmol/1. The relation between HX & pH was: (pH= -0.006HX + .735 (r=0.46, p=0.05). No baby received sodium bicarbonate. Conclusion: The present results demonstrating a good correlation between HX & BD is in agreement with animal studies. (Saugstad et al, 1978, Thiringer et al, 1980). Hypoxanthine determination is rapid & simple. HX more specifically than BD or lactate reflects tissue hypoxia. We therefore suggest that HX be measured routinely in clinical neonatology for assessment of hypoxia.
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