The metabolic response to different degrees of
hypoxia was studied in 14 lamb fetuses. We have previously found a substantial rise in the fetal arterial plasma
hypoxanthine (HX) level, in parallel with alterations of other
hypoxia indices during induced
asphyxia. Measurements of the arterio-venous (A-V) difference in the HX level across the CNS demonstrated a late efflux of this substance from the fetal brain, with a high resistance to
asphyxia. In this study, the effluxes of HX,
lactate, and in some cases
glucose, from the myocardium, liver, hindleg (skeletal muscle) and placenta were investigated in acutely exteriorised sheep fetuses with graded
asphyxia. The main findings were as follows: (a) myocardium: a release of HX early during
asphyxia, the magnitude of which paralelled the amount of mechanical work performed by the heart; a significant
lactate influx into the heart during normoxia and recovery period; (b) liver: hepatic HX release even during normoxia, increasing to substantial amounts in connection with increasing
asphyxia; (c) hindleg: release of HX only during the recovery period;
lactate efflux during all periods apart from severe
asphyxia, when an influx was seen for both substances; (d) placenta: production of
lactate during normoxia, and an efficient clearance of both
lactate and HX from the fetal plasma in combination with their concentration increasing during
asphyxia. It is concluded that the myocardium and liver are the main contributors to the elevated HX level during fetal
asphyxia among the fetal organs investigated, while skeletal muscle releases HX mostly during the period of reoxygenation.