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In the present study, chronically instrumented near\u2010term fetal sheep received surgical vagotomy (\n n<\/jats:italic>\n \u00a0=\u00a08) or sham vagotomy (control,\n n<\/jats:italic>\n \u00a0=\u00a011) to disable the peripheral chemoreflex and unmask myocardial hypoxia. One\u2010minute complete umbilical cord occlusions (UCOs) were performed every 2.5\u00a0min for 4\u00a0h or until arterial pressure fell below 20\u00a0mmHg. Hypotension and severe acidaemia developed progressively after 65.7\u00a0\u00b1\u00a07.2 UCOs in control fetuses and 49.5\u00a0\u00b1\u00a07.8 UCOs after vagotomy. Vagotomy was associated with faster development of metabolic acidaemia and faster impairment of arterial pressure during UCOs without impairing centralization of blood flow or neurophysiological adaptation to UCOs. During the first half of the UCO series, before severe hypotension developed, vagotomy was associated with a marked increase in FHR during UCOs. After the onset of evolving severe hypotension, FHR fell faster in control fetuses during the first 20\u00a0s of UCOs, but FHR during the final 40\u00a0s of UCOs became progressively more similar between groups, with no difference in the nadir of decelerations. In conclusion, FHR decelerations were initiated and sustained by the peripheral chemoreflex at a time when fetuses were able to maintain arterial pressure. After the onset of evolving hypotension and acidaemia, the peripheral chemoreflex continued to initiate decelerations, but myocardial hypoxia became progressively more important in sustaining and deepening decelerations.\n \n \n image<\/jats:alt-text>\n <\/jats:graphic>\n <\/jats:boxed-text>\n <\/jats:p>\n <\/jats:sec>\n \n Key points<\/jats:title>\n \n \n \n Brief repeated hypoxaemia during labour can trigger fetal heart rate decelerations by either the peripheral chemoreflex or myocardial hypoxia, but how this balance changes with fetal compromise is unknown.<\/jats:p>\n <\/jats:list-item>\n \n Reflex control of fetal heart rate was disabled by vagotomy to unmask the effects of myocardial hypoxia in chronically instrumented fetal sheep. Fetuses were then subjected to repeated brief hypoxaemia consistent with the rates of uterine contractions during labour.<\/jats:p>\n <\/jats:list-item>\n \n We show that the peripheral chemoreflex controls brief decelerations in their entirety at a time when fetuses were able to maintain normal or increased arterial pressure.<\/jats:p>\n <\/jats:list-item>\n \n The peripheral chemoreflex still initiated decelerations even after the onset of evolving hypotension and acidaemia, but myocardial hypoxia made an increasing contribution to sustain and deepen decelerations.<\/jats:p>\n <\/jats:list-item>\n <\/jats:list>\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1113\/jp284286","type":"journal-article","created":{"date-parts":[[2023,4,5]],"date-time":"2023-04-05T09:39:35Z","timestamp":1680687575000},"page":"2017-2041","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":22,"title":["Dissecting the contributions of the peripheral chemoreflex and myocardial hypoxia to fetal heart rate decelerations in near\u2010term fetal sheep"],"prefix":"10.1113","volume":"601","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8937-0846","authenticated-orcid":false,"given":"Christopher A.","family":"Lear","sequence":"first","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael J.","family":"Beacom","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simerdeep K.","family":"Dhillon","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0970-3063","authenticated-orcid":false,"given":"Benjamin A.","family":"Lear","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivia J.","family":"Mills","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark I.","family":"Gunning","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jenny A.","family":"Westgate","sequence":"additional","affiliation":[{"name":"Department of Obstetrics and Gynaecology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4336-7596","authenticated-orcid":false,"given":"Laura","family":"Bennet","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0656-7035","authenticated-orcid":false,"given":"Alistair J.","family":"Gunn","sequence":"additional","affiliation":[{"name":"The Fetal Physiology and Neuroscience Group, Department of Physiology The University of Auckland Auckland New Zealand"},{"name":"Department of Paediatrics Starship Children's Hospital Auckland New Zealand"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2023,4,19]]},"reference":[{"key":"e_1_2_5_2_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ejogrb.2018.02.026"},{"key":"e_1_2_5_3_1","doi-asserted-by":"publisher","DOI":"10.1007\/s13311-012-0108-y"},{"key":"e_1_2_5_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.ajog.2006.11.035"},{"key":"e_1_2_5_5_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0002-9378(13)70298-9"},{"key":"e_1_2_5_6_1","doi-asserted-by":"publisher","DOI":"10.1016\/0002-9378(92)91557-Q"},{"key":"e_1_2_5_7_1","volume-title":"Researches in prenatal life","author":"Barcroft J.","year":"1946"},{"key":"e_1_2_5_8_1","doi-asserted-by":"publisher","DOI":"10.1002\/cne.901350302"},{"issue":"3","key":"e_1_2_5_9_1","first-page":"292","article-title":"A study of fetal heart rate deceleration areas. 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