Antenatal dexamethasone after asphyxia increases neural injury in preterm fetal sheep
Maternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; however, its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the...
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| description | Maternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; however, its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the preterm brain.
Chronically instrumented singleton fetal sheep at 0.7 of gestation received asphyxia induced by complete umbilical cord occlusion for 25 minutes. 15 minutes after release of occlusion, ewes received a 3 ml i.m. injection of either dexamethasone (12 mg, n = 10) or saline (n = 10). Sheep were killed after 7 days recovery; survival of neurons in the hippocampus and basal ganglia, and oligodendrocytes in periventricular white matter were assessed using an unbiased stereological approach.
Maternal dexamethasone after asphyxia was associated with more severe loss of neurons in the hippocampus (CA3 regions, 290 ± 76 vs 484 ± 98 neurons/mm(2), mean ± SEM, P |
| doi_str_mv | 10.1371/journal.pone.0077480 |
| format | Article |
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Chronically instrumented singleton fetal sheep at 0.7 of gestation received asphyxia induced by complete umbilical cord occlusion for 25 minutes. 15 minutes after release of occlusion, ewes received a 3 ml i.m. injection of either dexamethasone (12 mg, n = 10) or saline (n = 10). Sheep were killed after 7 days recovery; survival of neurons in the hippocampus and basal ganglia, and oligodendrocytes in periventricular white matter were assessed using an unbiased stereological approach.
Maternal dexamethasone after asphyxia was associated with more severe loss of neurons in the hippocampus (CA3 regions, 290 ± 76 vs 484 ± 98 neurons/mm(2), mean ± SEM, P<0.05) and basal ganglia (putamen, 538 ± 112 vs 814 ± 34 neurons/mm(2), P<0.05) compared to asphyxia-saline, and with greater loss of both total (913 ± 77 vs 1201 ± 75/mm(2), P<0.05) and immature/mature myelinating oligodendrocytes in periventricular white matter (66 ± 8 vs 114 ± 12/mm(2), P<0.05, vs sham controls 165 ± 10/mm(2), P<0.001). This was associated with transient hyperglycemia (peak 3.5 ± 0.2 vs. 1.4 ± 0.2 mmol/L at 6 h, P<0.05) and reduced suppression of EEG power in the first 24 h after occlusion (maximum -1.5 ± 1.2 dB vs. -5.0 ± 1.4 dB in saline controls, P<0.01), but later onset and fewer overt seizures.
In preterm fetal sheep, exposure to maternal dexamethasone during recovery from asphyxia exacerbated brain damage.]]></description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0077480</identifier><identifier>PMID: 24204840</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Animals ; Anti-Inflammatory Agents - adverse effects ; Antibiotics ; Asphyxia ; Asphyxia - drug therapy ; Asphyxia - pathology ; Basal ganglia ; Basal Ganglia - drug effects ; Basal Ganglia - pathology ; Blood pressure ; Brain ; Brain damage ; Brain injury ; Cell Count ; Cell Death ; Cell survival ; Central nervous system depressants ; Cerebral blood flow ; Cerebral Ventricles - drug effects ; Cerebral Ventricles - pathology ; Dexamethasone ; Dexamethasone - adverse effects ; EEG ; Electrocardiography ; Electroencephalography ; Exposure ; Female ; Fetus ; Fetuses ; Ganglia ; Gestation ; Glucocorticoids ; Glucose ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - pathology ; Humidity ; Hyperglycemia ; Hypoxia ; Infant mortality ; Injections, Intramuscular ; Ischemia ; Morbidity ; Neonates ; Neurons ; Neurons - drug effects ; Neurons - pathology ; Newborn babies ; Occlusion ; Oligodendrocytes ; Oligodendroglia - drug effects ; Oligodendroglia - pathology ; Ovis aries ; Physiology ; Pregnancy ; Premature Birth - pathology ; Putamen ; Recovery ; Seizures ; Sheep ; Sheep, Domestic ; Steroids ; Steroids (Organic compounds) ; Studies ; Substantia alba ; Surgery ; Survival ; Traumatic brain injury ; Umbilical cord ; Umbilical Cord - pathology</subject><ispartof>PloS one, 2013-10, Vol.8 (10), p.e77480</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 Koome et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Koome et al 2013 Koome et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-b9159e44130177d7e253cc2d486a0ac2a3b851825cd5490b1fa05ff22e3e59663</citedby><cites>FETCH-LOGICAL-c692t-b9159e44130177d7e253cc2d486a0ac2a3b851825cd5490b1fa05ff22e3e59663</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799621/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799621/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2100,2926,23864,27922,27923,53789,53791,79370,79371</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24204840$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Sun, Kang</contributor><creatorcontrib>Koome, Miriam E</creatorcontrib><creatorcontrib>Davidson, Joanne O</creatorcontrib><creatorcontrib>Drury, Paul P</creatorcontrib><creatorcontrib>Mathai, Sam</creatorcontrib><creatorcontrib>Booth, Lindsea C</creatorcontrib><creatorcontrib>Gunn, Alistair Jan</creatorcontrib><creatorcontrib>Bennet, Laura</creatorcontrib><title>Antenatal dexamethasone after asphyxia increases neural injury in preterm fetal sheep</title><title>PloS one</title><addtitle>PLoS One</addtitle><description><![CDATA[Maternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; however, its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the preterm brain.
Chronically instrumented singleton fetal sheep at 0.7 of gestation received asphyxia induced by complete umbilical cord occlusion for 25 minutes. 15 minutes after release of occlusion, ewes received a 3 ml i.m. injection of either dexamethasone (12 mg, n = 10) or saline (n = 10). Sheep were killed after 7 days recovery; survival of neurons in the hippocampus and basal ganglia, and oligodendrocytes in periventricular white matter were assessed using an unbiased stereological approach.
Maternal dexamethasone after asphyxia was associated with more severe loss of neurons in the hippocampus (CA3 regions, 290 ± 76 vs 484 ± 98 neurons/mm(2), mean ± SEM, P<0.05) and basal ganglia (putamen, 538 ± 112 vs 814 ± 34 neurons/mm(2), P<0.05) compared to asphyxia-saline, and with greater loss of both total (913 ± 77 vs 1201 ± 75/mm(2), P<0.05) and immature/mature myelinating oligodendrocytes in periventricular white matter (66 ± 8 vs 114 ± 12/mm(2), P<0.05, vs sham controls 165 ± 10/mm(2), P<0.001). This was associated with transient hyperglycemia (peak 3.5 ± 0.2 vs. 1.4 ± 0.2 mmol/L at 6 h, P<0.05) and reduced suppression of EEG power in the first 24 h after occlusion (maximum -1.5 ± 1.2 dB vs. -5.0 ± 1.4 dB in saline controls, P<0.01), but later onset and fewer overt seizures.
In preterm fetal sheep, exposure to maternal dexamethasone during recovery from asphyxia exacerbated brain damage.]]></description><subject>Animals</subject><subject>Anti-Inflammatory Agents - adverse effects</subject><subject>Antibiotics</subject><subject>Asphyxia</subject><subject>Asphyxia - drug therapy</subject><subject>Asphyxia - pathology</subject><subject>Basal ganglia</subject><subject>Basal Ganglia - drug effects</subject><subject>Basal Ganglia - pathology</subject><subject>Blood pressure</subject><subject>Brain</subject><subject>Brain damage</subject><subject>Brain injury</subject><subject>Cell Count</subject><subject>Cell Death</subject><subject>Cell survival</subject><subject>Central nervous system depressants</subject><subject>Cerebral blood flow</subject><subject>Cerebral Ventricles - drug effects</subject><subject>Cerebral Ventricles - pathology</subject><subject>Dexamethasone</subject><subject>Dexamethasone - adverse effects</subject><subject>EEG</subject><subject>Electrocardiography</subject><subject>Electroencephalography</subject><subject>Exposure</subject><subject>Female</subject><subject>Fetus</subject><subject>Fetuses</subject><subject>Ganglia</subject><subject>Gestation</subject><subject>Glucocorticoids</subject><subject>Glucose</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - pathology</subject><subject>Humidity</subject><subject>Hyperglycemia</subject><subject>Hypoxia</subject><subject>Infant mortality</subject><subject>Injections, Intramuscular</subject><subject>Ischemia</subject><subject>Morbidity</subject><subject>Neonates</subject><subject>Neurons</subject><subject>Neurons - drug effects</subject><subject>Neurons - pathology</subject><subject>Newborn babies</subject><subject>Occlusion</subject><subject>Oligodendrocytes</subject><subject>Oligodendroglia - drug effects</subject><subject>Oligodendroglia - pathology</subject><subject>Ovis aries</subject><subject>Physiology</subject><subject>Pregnancy</subject><subject>Premature Birth - pathology</subject><subject>Putamen</subject><subject>Recovery</subject><subject>Seizures</subject><subject>Sheep</subject><subject>Sheep, Domestic</subject><subject>Steroids</subject><subject>Steroids (Organic compounds)</subject><subject>Studies</subject><subject>Substantia alba</subject><subject>Surgery</subject><subject>Survival</subject><subject>Traumatic brain injury</subject><subject>Umbilical cord</subject><subject>Umbilical Cord - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Koome, Miriam E</au><au>Davidson, Joanne O</au><au>Drury, Paul P</au><au>Mathai, Sam</au><au>Booth, Lindsea C</au><au>Gunn, Alistair Jan</au><au>Bennet, Laura</au><au>Sun, Kang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Antenatal dexamethasone after asphyxia increases neural injury in preterm fetal sheep</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-10-18</date><risdate>2013</risdate><volume>8</volume><issue>10</issue><spage>e77480</spage><pages>e77480-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract><![CDATA[Maternal glucocorticoid treatment for threatened premature delivery dramatically improves neonatal survival and short-term morbidity; however, its effects on neurodevelopmental outcome are variable. We investigated the effect of maternal glucocorticoid exposure after acute asphyxia on injury in the preterm brain.
Chronically instrumented singleton fetal sheep at 0.7 of gestation received asphyxia induced by complete umbilical cord occlusion for 25 minutes. 15 minutes after release of occlusion, ewes received a 3 ml i.m. injection of either dexamethasone (12 mg, n = 10) or saline (n = 10). Sheep were killed after 7 days recovery; survival of neurons in the hippocampus and basal ganglia, and oligodendrocytes in periventricular white matter were assessed using an unbiased stereological approach.
Maternal dexamethasone after asphyxia was associated with more severe loss of neurons in the hippocampus (CA3 regions, 290 ± 76 vs 484 ± 98 neurons/mm(2), mean ± SEM, P<0.05) and basal ganglia (putamen, 538 ± 112 vs 814 ± 34 neurons/mm(2), P<0.05) compared to asphyxia-saline, and with greater loss of both total (913 ± 77 vs 1201 ± 75/mm(2), P<0.05) and immature/mature myelinating oligodendrocytes in periventricular white matter (66 ± 8 vs 114 ± 12/mm(2), P<0.05, vs sham controls 165 ± 10/mm(2), P<0.001). This was associated with transient hyperglycemia (peak 3.5 ± 0.2 vs. 1.4 ± 0.2 mmol/L at 6 h, P<0.05) and reduced suppression of EEG power in the first 24 h after occlusion (maximum -1.5 ± 1.2 dB vs. -5.0 ± 1.4 dB in saline controls, P<0.01), but later onset and fewer overt seizures.
In preterm fetal sheep, exposure to maternal dexamethasone during recovery from asphyxia exacerbated brain damage.]]></abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24204840</pmid><doi>10.1371/journal.pone.0077480</doi><tpages>e77480</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2013-10, Vol.8 (10), p.e77480 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1442982348 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Animals Anti-Inflammatory Agents - adverse effects Antibiotics Asphyxia Asphyxia - drug therapy Asphyxia - pathology Basal ganglia Basal Ganglia - drug effects Basal Ganglia - pathology Blood pressure Brain Brain damage Brain injury Cell Count Cell Death Cell survival Central nervous system depressants Cerebral blood flow Cerebral Ventricles - drug effects Cerebral Ventricles - pathology Dexamethasone Dexamethasone - adverse effects EEG Electrocardiography Electroencephalography Exposure Female Fetus Fetuses Ganglia Gestation Glucocorticoids Glucose Hippocampus Hippocampus - drug effects Hippocampus - pathology Humidity Hyperglycemia Hypoxia Infant mortality Injections, Intramuscular Ischemia Morbidity Neonates Neurons Neurons - drug effects Neurons - pathology Newborn babies Occlusion Oligodendrocytes Oligodendroglia - drug effects Oligodendroglia - pathology Ovis aries Physiology Pregnancy Premature Birth - pathology Putamen Recovery Seizures Sheep Sheep, Domestic Steroids Steroids (Organic compounds) Studies Substantia alba Surgery Survival Traumatic brain injury Umbilical cord Umbilical Cord - pathology |
| title | Antenatal dexamethasone after asphyxia increases neural injury in preterm fetal sheep |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T23%3A18%3A02IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Antenatal%20dexamethasone%20after%20asphyxia%20increases%20neural%20injury%20in%20preterm%20fetal%20sheep&rft.jtitle=PloS%20one&rft.au=Koome,%20Miriam%20E&rft.date=2013-10-18&rft.volume=8&rft.issue=10&rft.spage=e77480&rft.pages=e77480-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0077480&rft_dat=%3Cgale_plos_%3EA478219251%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1442982348&rft_id=info:pmid/24204840&rft_galeid=A478219251&rft_doaj_id=oai_doaj_org_article_3880844cd506416493237e7dbb56d9cd&rfr_iscdi=true |