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Responses of the growth-retarded fetus to acute hypoxemia

  • Barry S.B. Block
    Footnotes
    Affiliations
    Department of Obstetrics and Gynecology, University of California (San Francisco) San Francisco, California USA.

    Department of Reproductive Sciences, University of California (San Francisco) San Francisco, California USA.

    the Cardiovascular Research Institute, University of California (San Francisco) San Francisco, California USA.
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  • Anibal J. Llanos
    Footnotes
    Affiliations
    Department of Obstetrics and Gynecology, University of California (San Francisco) San Francisco, California USA.

    Department of Reproductive Sciences, University of California (San Francisco) San Francisco, California USA.

    the Cardiovascular Research Institute, University of California (San Francisco) San Francisco, California USA.
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  • Robert K. Creasy
    Correspondence
    Reprint requests: Dr. R. K. Creasy, Department of Obstetrics, Gynecology and Reproductive Sciences, University of Texas Health Sciences Center at Houston, 6431 Fannin, Suite 3.270, Houston, Texas 77030.
    Affiliations
    Department of Obstetrics and Gynecology, University of California (San Francisco) San Francisco, California USA.

    Department of Reproductive Sciences, University of California (San Francisco) San Francisco, California USA.

    the Cardiovascular Research Institute, University of California (San Francisco) San Francisco, California USA.
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  • Author Footnotes
    ∗ Recipient of National Institutes of Health Research Service Award HL/HD 05964, Fellow in Maternal-Fetal Medicine.
    ∗∗ Recipient of a Fellowship from the Bay Area Health Association.
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      Abstract

      Growth retardation in the human fetus associated with maternal cardiovascular disease is frequently accompanied by birth asphyxia and perinatal mortality. We have investigated the cardiovascular responses to acute hypoxemia in the fetal lamb with growth retardation secondary to embolization of the uteroplacental vascular bed. In the basal period, fetal arterial PO2 and umbilical perfusion were significantly lower, and perfusion of the adrenal glands, brain, and heart was significantly higher, in embolized than in control fetal lambs. During imposed acute hypoxemia there was preferential perfusion of vital organs, the adrenal glands, brain, and heart in control and embolized fetuses. This preferential perfusion to the vital organs during hypoxemia was significantly more pronounced in embolized animals. Because of the increased compensation during acute hypoxemia, as reflected by the increased preferential perfusion of vital organs, the growth-retarded fetuses would probably decompensate sooner if the hypoxemia was prolonged.
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