<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>101(7)</volume><submitter>Ghesquiere L</submitter><pubmed_abstract>&lt;h4>Introduction&lt;/h4>This study evaluated the association between fetal heart rate variability (HRV) and the occurrence of hypoxic-ischemic encephalopathy in a fetal sheep model.&lt;h4>Material and methods&lt;/h4>The experimental protocol created a hypoxic condition with repeated cord occlusions in three phases (A, B, C) to achieve acidosis to pH &lt;7.00. Hemodynamic, gasometric and HRV parameters were analyzed during the protocol, and the fetal brain, brainstem and spinal cord were assessed histopathologically 48 h later. Associations between the various parameters and neural injury were compared between phases A, B and C using Spearman's rho test.&lt;h4>Results&lt;/h4>Acute anoxic-ischemic brain lesions in all regions was present in 7/9 fetuses, and specific neural injury was observed in 3/9 fetuses. The number of brainstem lesions correlated significantly and inversely with the HRV fetal stress index (r = -0.784; p = 0.021) in phase C and with HRV long-term variability (r = -0.677; p = 0.045) and short-term variability (r = -0.837; p = 0.005) in phase B. The number of neurological lesions did not correlate significantly with other markers of HRV.&lt;h4>Conclusions&lt;/h4>Neural injury caused by severe hypoxia was associated with HRV changes; in particular, brainstem damage was associated with changes in fetal-specific HRV markers.</pubmed_abstract><journal>Acta obstetricia et gynecologica Scandinavica</journal><pagination>758-770</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9564451</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Associations between fetal heart rate variability and umbilical cord occlusions-induced neural injury: An experimental study in a fetal sheep model.</pubmed_title><pmcid>PMC9564451</pmcid><pubmed_authors>Garabedian C</pubmed_authors><pubmed_authors>Nguyen S</pubmed_authors><pubmed_authors>Houfflin-Debarge V</pubmed_authors><pubmed_authors>De Jonckheere J</pubmed_authors><pubmed_authors>Perbet R</pubmed_authors><pubmed_authors>Lacan L</pubmed_authors><pubmed_authors>Hamoud Y</pubmed_authors><pubmed_authors>Sharma D</pubmed_authors><pubmed_authors>Ghesquiere L</pubmed_authors><pubmed_authors>Stichelbout M</pubmed_authors><pubmed_authors>Storme L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Associations between fetal heart rate variability and umbilical cord occlusions-induced neural injury: An experimental study in a fetal sheep model.</name><description>&lt;h4>Introduction&lt;/h4>This study evaluated the association between fetal heart rate variability (HRV) and the occurrence of hypoxic-ischemic encephalopathy in a fetal sheep model.&lt;h4>Material and methods&lt;/h4>The experimental protocol created a hypoxic condition with repeated cord occlusions in three phases (A, B, C) to achieve acidosis to pH &lt;7.00. Hemodynamic, gasometric and HRV parameters were analyzed during the protocol, and the fetal brain, brainstem and spinal cord were assessed histopathologically 48 h later. Associations between the various parameters and neural injury were compared between phases A, B and C using Spearman's rho test.&lt;h4>Results&lt;/h4>Acute anoxic-ischemic brain lesions in all regions was present in 7/9 fetuses, and specific neural injury was observed in 3/9 fetuses. The number of brainstem lesions correlated significantly and inversely with the HRV fetal stress index (r = -0.784; p = 0.021) in phase C and with HRV long-term variability (r = -0.677; p = 0.045) and short-term variability (r = -0.837; p = 0.005) in phase B. The number of neurological lesions did not correlate significantly with other markers of HRV.&lt;h4>Conclusions&lt;/h4>Neural injury caused by severe hypoxia was associated with HRV changes; in particular, brainstem damage was associated with changes in fetal-specific HRV markers.</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Jul</publication><modification>2025-04-04T23:44:30.263Z</modification><creation>2025-04-04T23:44:30.263Z</creation></dates><accession>S-EPMC9564451</accession><cross_references><pubmed>35502642</pubmed><doi>10.1111/aogs.14352</doi></cross_references></HashMap>