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First published online on March 10, 2005.
 Copyright © 2005 by The Physiological Society
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Received December 31, 2004
Revised January 25, 2005
Accepted after revision March 9, 2005

Anemia as a Programming agent in the Fetal Heart

lowell davis1*, Kent Thornburg1, and George Giraud1

1 oregon health sciences university

* To whom correspondence should be addressed. E-mail: davislo{at}ohsu.edu.

Summary: The intrauterine environment plays a powerful role in determining the life long risk of cardiovascular disease. A number of stressors are well known to affect the development of the cardiovascular system in utero including over/under maternal nutrition, excess glucocorticoid and chronic hypoxia. Chronic fetal anemia in sheep is a complex stressor that alters cardiac loading conditions, causes hypoxic stress and stimulates large changes in flow to specific tissues, including large increases in resting coronary blood flow and conductance. Decreased viscosity can account for approximately half of the increased flow. It appears that immature hearts are "plastic" in that increases in coronary conductance with fetal anemia persist into adulthood even if the anemia is corrected before birth. These large changes in conductance are possible only through extensive remodeling of the coronary tree. Adult hearts that were once anemic in utero are more resistant to hypoxic stress as adults but it is not known whether such an adaptation would be deleterious in later life. These studies indicate the need for investigation into the basic mechanisms of coronary tree remodeling in the immature myocardium. New information on these mechanisms would likely lead to better prevention of and therapies for adult-onset coronary disease


Key words: Development • Fetus • Heart




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