AJP - Regulatory, Integrative and Comparative Physiology, Vol 255, Issue 6 1049-R1054, Copyright © 1988 by American Physiological Society
Fetal cerebral responses to ventilation and oxygenation in utero
C. A. Gleason, M. D. Jones Jr, R. J. Traystman and R. H. Notter
Department of Pediatrics, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205.
Previous studies have shown that cerebral oxygen consumption (CMRO2)
increases by nearly 50% at birth. The perinatal factors responsible for
this increase are unknown; however, one possibility is that fetal CMRO2 is
constrained by the normal intrauterine arterial PO2 (PaO2) of approximately
20 mmHg. We investigated this possibility in seven near-term chronically
instrumented fetal sheep (131-138 days gestation) in which we inserted
vascular catheters and an endotracheal tube. After 1-3 days recovery, we
measured cerebral blood flow (CBF) with radiolabeled microspheres and
calculated CMRO2. Measurements were made in utero under three conditions
for each fetus: 1) nonventilated control; 2) ventilation with 3% O2-5%
CO2-92% N2; and 3) ventilation with an inspired oxygen concentration
sufficient to raise fetal PaO2 to normal newborn levels (mean 73 mmHg). A
calf lung surfactant extract (CLSE) was instilled into the endotracheal
tube of the fetus before ventilation to ensure adequate levels of alveolar
surfactant and to maintain stable pH and arterial PCO2. The results showed
that increasing fetal arterial PO2 to postnatal levels did not consistently
increase CMRO2. CBF decreased as arterial O2 content (CaO2) rose, with an
inverse hyperbolic response similar to that previously found to relate CBF
to CaO2 during fetal hypoxic hypoxia. This indicates that the normally low
intrauterine PaO2 does not intrinsically limit CMRO2 and implies that the
rapid increase in CMRO2 at birth reflects the activation of specific
cellular and physiological processes at (or near) this unique developmental
event.
