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Updated: May 22, 2026

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Instrumentation of Near-term Fetal Sheep for Multivariate Chronic Non-anesthetized Recordings
Published on: October 25, 2015
Renal sympathetic nerve activity during asphyxia in fetal sheep
Lindsea C Booth1, Simon C Malpas, Carolyn J Barrett
1Department of Physiology, The University of Auckland, Auckland, New Zealand.
Summary
Sympathetic nervous system (SNS) activity increases during fetal asphyxia, but renal sympathetic nerve activity (RSNA) is not the primary cause of reduced renal vascular conductance (RVC) in preterm sheep. Nonrenal sympathetic innervation is crucial for maintaining blood pressure near term.
Area of Science:
- Fetal Physiology
- Autonomic Nervous System Development
- Cardiovascular Adaptation
Background:
- The sympathetic nervous system (SNS) is vital for fetal adaptation to in utero stress like asphyxia.
- SNS responses mature late in gestation, but their role in asphyxia adaptation is not fully understood.
Purpose of the Study:
- To test if increased renal sympathetic nerve activity (RSNA) primarily causes decreased renal vascular conductance (RVC) during umbilical cord occlusion in preterm fetal sheep.
- To determine if near-term fetuses show a faster vasomotor response and greater RSNA increase compared to preterm fetuses.
Main Methods:
- Investigated fetal sheep at preterm (101 days) and near-term (119 days) stages.
- Induced complete umbilical cord occlusion to simulate asphyxia.
- Used surgical and chemical denervation to assess the causality of RSNA on RVC.
Main Results:
- All fetal sheep exhibited increased RSNA during occlusion; it was more sustained but not significantly greater in near-term fetuses.
- Near-term fetuses had a more rapid initial decrease in RVC that preceded the significant RSNA increase.
- Chemical denervation in near-term fetuses led to a drop in blood pressure, indicating critical nonrenal sympathetic roles.
Conclusions:
- RSNA increase is not the primary driver of RVC changes during fetal asphyxia, even at 0.7 gestation.
- By 0.8 gestation, sympathetic innervation of nonrenal vessels is essential for maintaining arterial blood pressure during acute asphyxia adaptation.
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