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(Hypertension. 2008;52:808.)
© 2008 American Heart Association, Inc.
Editorial Commentaries |
From the Departments of Obstetrics and Gynecology/Physiology, University of Alberta; and the Women and Childrens Health Research Institute, Edmonton, Alberta, Canada.
Correspondence to Sandra T. Davidge, 220 HMRC, University of Alberta, Edmonton, Alberta, Canada T6G 2S2. E-mail sandra.davidge@ualberta.ca
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
In this issue of Hypertension, Yzydorczyk et a11 present a novel approach to investigate how adverse environmental conditions during the early stages of life can lead to cardiovascular complications during adulthood. The authors used a model in which newborn rats were exposed to 80% oxygen from postnatal days 3 to 10. Although the rats used in the study were born at term, the authors suggest that, in some respects, their developmental stage is equivalent to that of a preterm fetus, allowing some aspects, such as kidney, lung, and vascular development, to be related to premature infants. Therefore, the approach taken by Yzydorczyk et al1 also provides additional clinical significance to their findings that may have implications in the care of premature babies in neonatal intensive care units and the use of oxygen therapy.
The ability of organisms to adapt to certain environmental conditions by permanently changing key functional elements is a fascinating concept that has been with us for a long time. One of the events that popularized this "programming" concept was the publishing of an article by Barker and Osmond2 in the early 1980s that demonstrated an association between low birth weight and an increment in standardized mortality rates later in life. During the following decades, other epidemiological studies linked adverse conditions during fetal stages and early childhood with adverse health outcomes later in life, including coronary heart disease, stroke, type 2 diabetes mellitus, and metabolic syndrome.3 Also known as the "fetal origins of adult disease" theory, this
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