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Repetitive reduction of uterine blood flow and its influence on fetal transcutaneous PO2 and cardiovascular variables.

The influence of repeated asphyxia on fetal transcutaneous PO2, relative local skin perfusion, heart rate, blood gases and pH was investigated in 15 experiments on 8 acutely instrumented sheep fetuses in utero between 125 and 145 days gestation (term is 147 days). Uterine blood flow was intermittently arrested (11 times within 33 min) by intra-vascular maternal aortic occlusion, exposing the fetuses to repeated episodes of asphyxia of 30 (n = 3), 60 (n = 9) and 90 (n = 3) s duration. The fetal transcutaneous PO2 fell as the duration of asphyxia (2 alpha less than 0.01), heart rate deceleration area (2 alpha less than 0.01) and acidaemia (2 alpha less than 0.01) increased. With decreasing skin perfusion, which was dependent on the duration of asphyxia (2 alpha less than 0.001) and acidaemia (2 alpha less than 0.001), a discrepancy developed between transcutaneous and arterial PO2. The increase (delta) in transcutaneous-arterial PO2 difference was related linearly to the duration of asphyxia (2 alpha less than 0.01), the mean haemoglobin oxygen saturation (2 alpha less than 0.001), acidaemia (2 alpha less than 0.001) and relative local skin flow (2 alpha less than 0.05). It was highest after severe episodes of asphyxia (90 s), when O2 saturation, skin blood flow and arterial blood pH values were low. Fetal heart rate deceleration area was only correlated with the cutaneous-arterial PO2 difference when the mean fetal haemoglobin oxygen saturation was below 35%. Thus, a discrimination of heart rate decelerations that are significant for the fetus seems to be possible, when associated with low transcutaneous PO2 values. We conclude that in the sheep fetus transcutaneous PO2 measurements during repeated asphyxial episodes yield information on fetal oxygenation and on the skin vasomotor response.