The peripheral chemoreflex: indefatigable guardian of fetal physiological adaptation to labour

Christopher A. Lear, Guido Wassink, Jenny A. Westgate, Jan Nijhuis, Austin Ugwumadu, Robert Galinsky, Laura Bennet, Alistair J Gunn

Research output: Contribution to journalReview ArticleResearchpeer-review

Abstract

The fetus is consistently exposed to repeated periods of impaired oxygen (hypoxaemia) and nutrient supply in labour. This is balanced by the healthy fetus's remarkable anaerobic tolerance and impressive ability to mount protective adaptations to hypoxaemia. The most important mediator of fetal adaptations to brief repeated hypoxaemia is the peripheral chemoreflex, a rapid reflex response to acute falls in arterial oxygen tension. The overwhelming majority of fetuses are able to respond to repeated uterine contractions without developing hypotension or hypoxic–ischaemic injury. In contrast, fetuses who are either exposed to severe hypoxaemia, for example during uterine hyperstimulation, or enter labour with reduced anaerobic reserve (e.g. as shown by severe fetal growth restriction) are at increased risk of developing intermittent hypotension and cerebral hypoperfusion. It is remarkable to note that when fetuses develop hypotension during such repeated severe hypoxaemia, it is not mediated by impaired reflex adaptation, but by failure to maintain combined ventricular output, likely due to a combination of exhaustion of myocardial glycogen and evolving myocardial injury. The chemoreflex is suppressed by relatively long periods of severe hypoxaemia of 1.5–2 min, longer than the typical contraction. Even in this setting, the peripheral chemoreflex is consistently reactivated between contractions. These findings demonstrate that the peripheral chemoreflex is an indefatigable guardian of fetal adaptation to labour.
Original languageEnglish
Pages (from-to)5611-5623
Number of pages13
JournalThe Journal of Physiology
Volume596
Issue number23
DOIs
Publication statusPublished - 1 Dec 2018
Externally publishedYes

Cite this

Lear, C. A., Wassink, G., Westgate, J. A., Nijhuis, J., Ugwumadu, A., Galinsky, R., ... Gunn, A. J. (2018). The peripheral chemoreflex: indefatigable guardian of fetal physiological adaptation to labour. The Journal of Physiology, 596(23), 5611-5623. https://doi.org/10.1113/JP274937
Lear, Christopher A. ; Wassink, Guido ; Westgate, Jenny A. ; Nijhuis, Jan ; Ugwumadu, Austin ; Galinsky, Robert ; Bennet, Laura ; Gunn, Alistair J. / The peripheral chemoreflex : indefatigable guardian of fetal physiological adaptation to labour. In: The Journal of Physiology. 2018 ; Vol. 596, No. 23. pp. 5611-5623.
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Lear, CA, Wassink, G, Westgate, JA, Nijhuis, J, Ugwumadu, A, Galinsky, R, Bennet, L & Gunn, AJ 2018, 'The peripheral chemoreflex: indefatigable guardian of fetal physiological adaptation to labour' The Journal of Physiology, vol. 596, no. 23, pp. 5611-5623. https://doi.org/10.1113/JP274937

The peripheral chemoreflex : indefatigable guardian of fetal physiological adaptation to labour. / Lear, Christopher A.; Wassink, Guido; Westgate, Jenny A.; Nijhuis, Jan; Ugwumadu, Austin; Galinsky, Robert; Bennet, Laura; Gunn, Alistair J.

In: The Journal of Physiology, Vol. 596, No. 23, 01.12.2018, p. 5611-5623.

Research output: Contribution to journalReview ArticleResearchpeer-review

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T1 - The peripheral chemoreflex

T2 - indefatigable guardian of fetal physiological adaptation to labour

AU - Lear, Christopher A.

AU - Wassink, Guido

AU - Westgate, Jenny A.

AU - Nijhuis, Jan

AU - Ugwumadu, Austin

AU - Galinsky, Robert

AU - Bennet, Laura

AU - Gunn, Alistair J

PY - 2018/12/1

Y1 - 2018/12/1

N2 - The fetus is consistently exposed to repeated periods of impaired oxygen (hypoxaemia) and nutrient supply in labour. This is balanced by the healthy fetus's remarkable anaerobic tolerance and impressive ability to mount protective adaptations to hypoxaemia. The most important mediator of fetal adaptations to brief repeated hypoxaemia is the peripheral chemoreflex, a rapid reflex response to acute falls in arterial oxygen tension. The overwhelming majority of fetuses are able to respond to repeated uterine contractions without developing hypotension or hypoxic–ischaemic injury. In contrast, fetuses who are either exposed to severe hypoxaemia, for example during uterine hyperstimulation, or enter labour with reduced anaerobic reserve (e.g. as shown by severe fetal growth restriction) are at increased risk of developing intermittent hypotension and cerebral hypoperfusion. It is remarkable to note that when fetuses develop hypotension during such repeated severe hypoxaemia, it is not mediated by impaired reflex adaptation, but by failure to maintain combined ventricular output, likely due to a combination of exhaustion of myocardial glycogen and evolving myocardial injury. The chemoreflex is suppressed by relatively long periods of severe hypoxaemia of 1.5–2 min, longer than the typical contraction. Even in this setting, the peripheral chemoreflex is consistently reactivated between contractions. These findings demonstrate that the peripheral chemoreflex is an indefatigable guardian of fetal adaptation to labour.

AB - The fetus is consistently exposed to repeated periods of impaired oxygen (hypoxaemia) and nutrient supply in labour. This is balanced by the healthy fetus's remarkable anaerobic tolerance and impressive ability to mount protective adaptations to hypoxaemia. The most important mediator of fetal adaptations to brief repeated hypoxaemia is the peripheral chemoreflex, a rapid reflex response to acute falls in arterial oxygen tension. The overwhelming majority of fetuses are able to respond to repeated uterine contractions without developing hypotension or hypoxic–ischaemic injury. In contrast, fetuses who are either exposed to severe hypoxaemia, for example during uterine hyperstimulation, or enter labour with reduced anaerobic reserve (e.g. as shown by severe fetal growth restriction) are at increased risk of developing intermittent hypotension and cerebral hypoperfusion. It is remarkable to note that when fetuses develop hypotension during such repeated severe hypoxaemia, it is not mediated by impaired reflex adaptation, but by failure to maintain combined ventricular output, likely due to a combination of exhaustion of myocardial glycogen and evolving myocardial injury. The chemoreflex is suppressed by relatively long periods of severe hypoxaemia of 1.5–2 min, longer than the typical contraction. Even in this setting, the peripheral chemoreflex is consistently reactivated between contractions. These findings demonstrate that the peripheral chemoreflex is an indefatigable guardian of fetal adaptation to labour.

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