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The effect of hypoxia in development.
Birth Defects Res C Embryo Today. 2007 Sep; 81(3):215-28.BD

Abstract

There is increasing evidence that the oxygen supply to the human embryo in the first trimester is tightly controlled, suggesting that too much oxygen may interfere with development. The use of hypoxia probes in mammalian embryos during the organogenic period indicates that the embryo is normally in a state of partial hypoxia, and this may be essential to control cardiovascular development, perhaps under the control of hypoxia-inducible factor (HIF). A consequence of this state of partial hypoxia is that disturbances in the oxygen supply can more easily lead to a damaging degree of hypoxia. Experimental mammalian embryos show a surprising degree of resilience to hypoxia, with many organogenic stage embryos able to survive 30-60 min of anoxia. However, in some embryos this degree of hypoxia causes abnormal development, particularly transverse limb reduction defects. These abnormalities are preceded by hemorrhage/edema and tissue necrosis. Other parts of the embryo are also susceptible to this hypoxia-induced damage and include the genital tubercle, the developing nose, the tail, and the central nervous system. Other frequently observed defects in animal models of prenatal hypoxia include cleft lip, maxillary hypoplasia, and heart defects. Animal studies indicate that hypoxic episodes in the first trimester of human pregnancy could occur by temporary constriction of the uterine arteries. This could be a consequence of exposure to cocaine, misoprostol, or severe shock, and there is evidence that these exposures have resulted in hypoxia-related malformations in the human. Exposure to drugs that block the potassium current (IKr) can cause severe slowing and arrhythmia of the mammalian embryonic heart and consequently hypoxia in the embryo. These drugs are highly teratogenic in experimental animals. There is evidence that drugs with IKr blockade as a side effect, for example phenytoin, may cause birth defects in the human by causing periods of embryonic hypoxia. The strongest evidence of hypoxia causing birth defects in the human comes from studies of fetuses lacking hemoglobin (Hb) F. These fetuses are thought to be hypoxic from about the middle of the first trimester and show a range of birth defects, particularly transverse limb reduction defects.

Authors+Show Affiliations

Department of Anatomy and Histology, University of Sydney, Sydney, Australia. billweb@anatomy.usyd.edu.auNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

17963271

Citation

Webster, William S., and Dominique Abela. "The Effect of Hypoxia in Development." Birth Defects Research. Part C, Embryo Today : Reviews, vol. 81, no. 3, 2007, pp. 215-28.
Webster WS, Abela D. The effect of hypoxia in development. Birth Defects Res C Embryo Today. 2007;81(3):215-28.
Webster, W. S., & Abela, D. (2007). The effect of hypoxia in development. Birth Defects Research. Part C, Embryo Today : Reviews, 81(3), 215-28.
Webster WS, Abela D. The Effect of Hypoxia in Development. Birth Defects Res C Embryo Today. 2007;81(3):215-28. PubMed PMID: 17963271.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The effect of hypoxia in development. AU - Webster,William S, AU - Abela,Dominique, PY - 2007/10/30/pubmed PY - 2007/12/14/medline PY - 2007/10/30/entrez SP - 215 EP - 28 JF - Birth defects research. Part C, Embryo today : reviews JO - Birth Defects Res. C Embryo Today VL - 81 IS - 3 N2 - There is increasing evidence that the oxygen supply to the human embryo in the first trimester is tightly controlled, suggesting that too much oxygen may interfere with development. The use of hypoxia probes in mammalian embryos during the organogenic period indicates that the embryo is normally in a state of partial hypoxia, and this may be essential to control cardiovascular development, perhaps under the control of hypoxia-inducible factor (HIF). A consequence of this state of partial hypoxia is that disturbances in the oxygen supply can more easily lead to a damaging degree of hypoxia. Experimental mammalian embryos show a surprising degree of resilience to hypoxia, with many organogenic stage embryos able to survive 30-60 min of anoxia. However, in some embryos this degree of hypoxia causes abnormal development, particularly transverse limb reduction defects. These abnormalities are preceded by hemorrhage/edema and tissue necrosis. Other parts of the embryo are also susceptible to this hypoxia-induced damage and include the genital tubercle, the developing nose, the tail, and the central nervous system. Other frequently observed defects in animal models of prenatal hypoxia include cleft lip, maxillary hypoplasia, and heart defects. Animal studies indicate that hypoxic episodes in the first trimester of human pregnancy could occur by temporary constriction of the uterine arteries. This could be a consequence of exposure to cocaine, misoprostol, or severe shock, and there is evidence that these exposures have resulted in hypoxia-related malformations in the human. Exposure to drugs that block the potassium current (IKr) can cause severe slowing and arrhythmia of the mammalian embryonic heart and consequently hypoxia in the embryo. These drugs are highly teratogenic in experimental animals. There is evidence that drugs with IKr blockade as a side effect, for example phenytoin, may cause birth defects in the human by causing periods of embryonic hypoxia. The strongest evidence of hypoxia causing birth defects in the human comes from studies of fetuses lacking hemoglobin (Hb) F. These fetuses are thought to be hypoxic from about the middle of the first trimester and show a range of birth defects, particularly transverse limb reduction defects. SN - 1542-975X UR - https://www.unboundmedicine.com/medline/citation/17963271/The_effect_of_hypoxia_in_development_ L2 - https://doi.org/10.1002/bdrc.20102 DB - PRIME DP - Unbound Medicine ER -