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NeoReviews Vol.7 No.4 2006 e189
© 2006 American Academy of Pediatrics

An Obstetric Point of View on Fetal Adaptation and Reprogramming

^* Professor, Department of Obstetrics and Gynecology, Physiology and Pharmacology and of Pediatrics, University of Western Ontario, London, Ontario, Canada

The first 300 words of the full text of this article appear below.

	Objectives

 
After completing this article, readers should be able to:

1. Define the difference between fetal adaptation and fetal programming.
   
2. Describe the mechanisms involved in maintaining fetal oxygenation.
   
3. Describe how maternal glycemic control affects fetal growth and development.
   
4. List the known stimuli involved in fetal programming in humans.
   

	Adaptation and Reprogramming

 
For pregnant women who want to have healthy babies and their obstetricians, the period extending from several weeks prior to conception until birth is of obvious interest. Problems affecting pregnancy may have consequences on the developing fetus resulting from adaptation or reprogramming. An adaptation is the action or process of adapting or being adapted. Adaptation implies a change by which an organism becomes better suited to its environment. Programming describes the mechanisms by which a stimulus or insult at a critical period of development has lasting or lifelong effects.

	Fetal Adaptation to Hypoxia and Hyperglycemia

 
Pregnancy affects all the determinants of oxygen delivery to the uteroplacental circulation. Maternal ventilation increases, which normally does not change arterial O₂ saturation, although mild respiratory alkalosis ensues. Maternal hemoglobin concentrations decline due to greater expansion of plasma than red cell mass and reduced arterial O₂ content. A rise in uteroplacental blood flow is due to higher cardiac output and redistribution of blood flow to favor uteroplacental circulation. Maternal cardiac output increases as a result of a decrease in systemic vascular resistance that begins in the luteal phase immediately following conception and an increase in blood volume.

The fetus lives and grows in a relatively "hypoxic" environment compared with the adult. The fetal arterial PO₂ is approximately 20 mm Hg compared with approximately 80 mm Hg in adults. The low fetal arterial PO₂ can be attributed largely to the venous equilibration of placental gas exchange in which both maternal uterine venous and fetal umbilical venous vasculature streams run in the same direction and . . . [Full Text of this Article]

This article has been cited by other articles:

				J. Gosselin, J.-C. Fouron, and C. Amiel-Tison Consequences of Uteroplacental Insufficiency on Developmental and Intellectual Performances NeoReviews, April 1, 2006; 7(4): e202 - e207. [Full Text] [PDF]