Our aim was to determine the effects of 12 h of hypoxaemia on cerebral blood flow (CBF) and cerebral O2 delivery in ovine fetuses at 0.6 gestation. During fetal hypoxaemia, induced by reduced uterine blood flow, fetal SaO2 and PaO2 were reduced (p < 0.01) from control values of 77.0 ± 1.6% and 27.3 ± 1.0 mm Hg, respectively, to 28.4 ± 3.4% and 15.6 ± 0.6 mm Hg; fetal pHa decreased from control values of 7.37 ± 0.01 to 7.20 ± 0.02 at 3 h, but returned to control values before 12 h. CBF (ml/min/100 g) was 2.0- to 2.6-fold higher (p < 0.01) than control values during hypoxaemia, but only 1.7-fold higher (p < 0.01) at 3 h when pHa was lowest. Cerebral O2 delivery (ml/min/100g) was lower (p < 0.01) than control values of 3.15 ± 0.29 at 1.5 h (2.09 ± 0.36) and 3 h (1.84 ± 0.22) of hypoxaemia and higher 1 h after hypoxaemia had ceased (3.81 ± 0.22, p < 0.01). We conclude that the ovine fetus at 0.6 gestation is unable to sustain increased CBF and hence maintain cerebral O2 delivery during the first 6 h of hypoxaemia, a time which coincides with acidaemia; in contrast, at 6 and 12 h of hypoxaemia, when pHa was normal, cerebral O2 delivery was similar to control values. Reduced cerebral O2 delivery during the early, acidaemic, stages of hypoxaemia may lead to impaired neural development.

Keywords:
Preterm fetus, ovine, Hypoxia, Acidaemia, Coloured microspheres, Cerebral blood flow, Cerebral oxygen delivery
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© 1997 S. Karger AG, Basel
1997
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