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This Article Full Text Full Text (PDF) All Versions of this Article: 563/2/611    most recent jphysiol.2004.080523v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Danielson, L. Articles by Morrison, J. L Search for Related Content PubMed PubMed Citation Articles by Danielson, L. Articles by Morrison, J. L

¹ Centre for the Early Origins of Adult Health, Discipline of Physiology, School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, SA 5005, Australia

Placental insufficiency resulting in restriction of fetal substrate supply and fetal hypoxaemia is a major cause of restricted fetal growth and increased neonatal morbidity. Fetal adaptations to placental restriction (PR) include increases in circulating catecholamines and cortisol and decreased fetal body growth, with relative sparing of brain growth. The mechanisms underlying the redistribution of fetal cardiac output in PR fetuses are not known and the aim of this study was to determine whether maintenance of fetal blood pressure (BP) in the PR fetus is dependent on -adrenergic stimulation. PR was induced by removing the majority of uterine caruncles in the ewe before conception. Sterile vascular surgery was performed on seven PR and six control fetuses at 113–120 days' gestation (term = 150 ± 3 days). Fetuses with a mean arterial P_O2 < 17 mmHg between 123 and 127 days' gestation were defined as hypoxic. There was a greater fall (P < 0.05) in fetal BP during phentolamine infusion (I.V: 5 mg bolus, 0.2 mg kg^–1 min^–1 for 2 h) in the hypoxic PR group (–15 ± 2 mmHg) compared with normoxic controls (–5 ± 1 mmHg). The fall in fetal BP during phentolamine infusion was directly related to the level of fetal P_O2. Fetal BP and HR responses to phenylephrine (I.V.: 40 µg kg^–1) were not different between PR and control fetuses. The maintenance of BP in the chronically hypoxic fetus is therefore dependent on -adrenergic activation, and this fetal adaptation to a suboptimal intrauterine environment pre-dates the development of significant growth restriction. While this adaptation may play a critical role in the redistribution of fetal cardiac output to ensure the sparing of brain growth, it may have adverse consequences for peripheral vascular function in the neonatal period and in adult life.

(Received 2 December 2004; accepted after revision 11 January 2005; first published online 13 January 2005)
Corresponding author J. Morrison: Fourth Floor, Medical School South, Discipline of Physiology, School of Molecular and Biomedical Sciences, University of Adelaide, Adelaide, SA 5000 Australia. Email: janna.morrison{at}adelaide.edu.au

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