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Title: Fetal cerebral responses to ventilation and oxygenation in utero

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:6036836
; ; ;  [1]
  1. Johns Hopkins Univ. School of Medicine, Baltimore, MD (USA) Univ. of Rochester School of Medicine and Dentistry, NY (USA)

Previous studies have shown that cerebral oxygen consumption (CMRO{sub 2}) increases by nearly 50% at birth. The perinatal factors responsible for this increase are unknown; however, one possibility is that fetal CMRO{sub 2} is constrained by the normal intrauterine arterial Po{sub 2} (Pa{sub 0{sub 2}}) of {approximately}20 mmHg. The authors investigated this possibility in seven near-term chronically instrumented fetal sheep (131-138 days gestation) in which they inserted vascular catheters and an endotracheal tube. After 1-3 days recovery, they measured cerebral blood flow (CBF) with radiolabeled microspheres and calculated CMRO{sub 2}. Measurements were made in utero under three conditions for each fetus: (1) nonventilated control; (2) ventilation with 3% O{sub 2}-5% CO{sub 2}-92% N{sub 2}; and (3) ventilation with an inspired oxygen concentration sufficient to raise fetal Pa{sub 0{sub 2}} to normal newborn levels. The results showed that increasing fetal arterial Po{sub 2} to postnatal levels did not consistently increase CMRO{sub 2}. CBF decreased as arterial O{sub 2} content (Ca{sub 0{sub 2}}) rose, with an inverse hyperbolic response similar to that previously found to relate CBF to Ca{sub 0{sub 2}} during fetal hypoxic hypoxia. This indicates that the normally low intrauterine Pa{sub 0{sub 2}} does not intrinsically limit CMRO{sub 2} and implies that the rapid increase in CMRO{sub 2} at birth reflects the activation of specific cellular and physiological processes at (or near) this unique developmental event.

OSTI ID:
6036836
Journal Information:
American Journal of Physiology; (USA), Vol. 255:6; ISSN 0002-9513
Country of Publication:
United States
Language:
English

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