Cholinergic and β-adrenergic control of cardiovascular reflex responses to brief repeated asphyxia in term-equivalent fetal sheep

Robert Galinsky, Christopher A. Lear, Kyohei Yamaguchi, Guido Wassink, Jennifer A. Westgate, Laura Bennet, Alistair J. Gunn

Research output: Contribution to journalArticleResearchpeer-review

Abstract

The role of cholinergic and β-adrenergic activity in mediating fetal cardiovascular recovery from brief repeated episodes of asphyxia, consistent with established labor, remains unclear. In this study, we tested the effect of cholinergic and β-adrenergic blockade on the fetal chemoreflex and fetal heart rate (FHR) overshoot responses during brief repeated asphyxia at rates consistent with early or active labor. Chronically instrumented fetal sheep at 0.85 of gestation received either intravenous atropine sulfate (cholinergic blockade; n = 7) or vehicle (n = 8) followed by 3 × 1-min umbilical cord occlusions repeated every 5 min (1:5; consistent with early labor), or intravenous propranolol hydrochloride (β-adrenergic blockade; n = 8) or vehicle (n = 6) followed by 3 × 2-min occlusions repeated every 5 min (2:5; consistent with active labor). In vehicle controls, 1:5 occlusions were associated with rapid and sustained FHR decelerations followed by rapid return of FHR to baseline values after release of the occlusion. Cholinergic blockade abolished FHR decelerations during occlusions and caused FHR overshoot after release of the occlusion (P < 0.05 vs. control 1:5). In vehicle controls, 2:5 occlusions caused rapid and sustained FHR decelerations followed by FHR overshoot after release of the occlusion. β-adrenergic blockade was associated with greater reduction in FHR during occlusions and attenuated FHR overshoot (P < 0.05 vs. control 2:5). These data demonstrate that the FHR overshoot pattern after asphyxia is mediated by a combination of attenuated parasympathetic activity and increased β-adrenergic stimulation of the fetal heart.

Original languageEnglish
Pages (from-to)R949-R956
Number of pages8
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume311
Issue number5
DOIs
Publication statusPublished - 10 Nov 2016
Externally publishedYes

Keywords

  • Autonomic nervous system
  • Chemoreflex
  • Fetal asphyxia

Cite this

Galinsky, Robert ; Lear, Christopher A. ; Yamaguchi, Kyohei ; Wassink, Guido ; Westgate, Jennifer A. ; Bennet, Laura ; Gunn, Alistair J. / Cholinergic and β-adrenergic control of cardiovascular reflex responses to brief repeated asphyxia in term-equivalent fetal sheep. In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology. 2016 ; Vol. 311, No. 5. pp. R949-R956.
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Cholinergic and β-adrenergic control of cardiovascular reflex responses to brief repeated asphyxia in term-equivalent fetal sheep. / Galinsky, Robert; Lear, Christopher A.; Yamaguchi, Kyohei; Wassink, Guido; Westgate, Jennifer A.; Bennet, Laura; Gunn, Alistair J.

In: American Journal of Physiology - Regulatory Integrative and Comparative Physiology, Vol. 311, No. 5, 10.11.2016, p. R949-R956.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Lear, Christopher A.

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AB - The role of cholinergic and β-adrenergic activity in mediating fetal cardiovascular recovery from brief repeated episodes of asphyxia, consistent with established labor, remains unclear. In this study, we tested the effect of cholinergic and β-adrenergic blockade on the fetal chemoreflex and fetal heart rate (FHR) overshoot responses during brief repeated asphyxia at rates consistent with early or active labor. Chronically instrumented fetal sheep at 0.85 of gestation received either intravenous atropine sulfate (cholinergic blockade; n = 7) or vehicle (n = 8) followed by 3 × 1-min umbilical cord occlusions repeated every 5 min (1:5; consistent with early labor), or intravenous propranolol hydrochloride (β-adrenergic blockade; n = 8) or vehicle (n = 6) followed by 3 × 2-min occlusions repeated every 5 min (2:5; consistent with active labor). In vehicle controls, 1:5 occlusions were associated with rapid and sustained FHR decelerations followed by rapid return of FHR to baseline values after release of the occlusion. Cholinergic blockade abolished FHR decelerations during occlusions and caused FHR overshoot after release of the occlusion (P < 0.05 vs. control 1:5). In vehicle controls, 2:5 occlusions caused rapid and sustained FHR decelerations followed by FHR overshoot after release of the occlusion. β-adrenergic blockade was associated with greater reduction in FHR during occlusions and attenuated FHR overshoot (P < 0.05 vs. control 2:5). These data demonstrate that the FHR overshoot pattern after asphyxia is mediated by a combination of attenuated parasympathetic activity and increased β-adrenergic stimulation of the fetal heart.

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