A piglet survival model of posthypoxic encephalopathy

The aim of this study was to produce a neonatal piglet model which, avoiding vessel ligation, exposed the whole animal to hypoxia and produced dose-dependent clinical encephalopathy and neuropathologic damage similar to that seen after birth asphyxia. Twenty-three piglets were halothane-anesthetized...

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Veröffentlicht in:Pediatric research 1996-11, Vol.40 (5), p.738-748
Hauptverfasser: THORESEN, M, HAALAND, K, LØBERG, E. M, WHITELAW, A, APRICENA, F, HANKØ, E, STEEN, P. A
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container_end_page 748
container_issue 5
container_start_page 738
container_title Pediatric research
container_volume 40
creator THORESEN, M
HAALAND, K
LØBERG, E. M
WHITELAW, A
APRICENA, F
HANKØ, E
STEEN, P. A
description The aim of this study was to produce a neonatal piglet model which, avoiding vessel ligation, exposed the whole animal to hypoxia and produced dose-dependent clinical encephalopathy and neuropathologic damage similar to that seen after birth asphyxia. Twenty-three piglets were halothane-anesthetized. Hypoxia was induced in 19 piglets by reducing the fractional concentration of inspired oxygen (FiO2) to the maximum concentration at which the EEG amplitude was below 7 microV (low amplitude) for 17-55 min. There were transient increases in Fio2 to correct bradycardia and hypotension. Posthypoxia, the piglets were extubated when breathing was stable. Four were sham-treated controls. We aimed at 72-h survival; seven died prematurely due to posthypoxic complications. EEG and a videotaped itemized neurologic assessment were recorded regularly. We found that 95% of the animals showed neuropathologic damage. The duration of low amplitude EEG during the insult and the arterial pH at the end of the insult correlated with cortical/white matter damage; r = 0.75 and 0.81, respectively. Early postinsult EEG background amplitude (r = 0.86 at 3 h) and neurologic score (r = 0.79 at 8 h) correlated with neuropathology. Epileptic seizures in seven animals were always associated with severe neuropathologic damage. We conclude that EEG-controlled hypoxia and subsequent intensive care enabled the animals to survive with an encephalopathy which correlated with the cerebral hypoxic insult. The encephalopathy was clinically, electrophysiologically, and neuropathologically similar to that in the asphyxiated term infant. This model is suitable for examining mechanisms of damage and evaluation of potential protective therapies after birth asphyxia.
doi_str_mv 10.1203/00006450-199611000-00014
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EEG and a videotaped itemized neurologic assessment were recorded regularly. We found that 95% of the animals showed neuropathologic damage. The duration of low amplitude EEG during the insult and the arterial pH at the end of the insult correlated with cortical/white matter damage; r = 0.75 and 0.81, respectively. Early postinsult EEG background amplitude (r = 0.86 at 3 h) and neurologic score (r = 0.79 at 8 h) correlated with neuropathology. Epileptic seizures in seven animals were always associated with severe neuropathologic damage. We conclude that EEG-controlled hypoxia and subsequent intensive care enabled the animals to survive with an encephalopathy which correlated with the cerebral hypoxic insult. The encephalopathy was clinically, electrophysiologically, and neuropathologically similar to that in the asphyxiated term infant. 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Obstetrics ; Heart - physiopathology ; Humans ; Hypoxia - pathology ; Hypoxia - physiopathology ; Infant, Newborn ; Kidney - pathology ; Liver - pathology ; Lung - pathology ; Medical sciences ; Swine</subject><ispartof>Pediatric research, 1996-11, Vol.40 (5), p.738-748</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,782,786,27931,27932</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=2495897$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8910940$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>THORESEN, M</creatorcontrib><creatorcontrib>HAALAND, K</creatorcontrib><creatorcontrib>LØBERG, E. 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A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A piglet survival model of posthypoxic encephalopathy</atitle><jtitle>Pediatric research</jtitle><addtitle>Pediatr Res</addtitle><date>1996-11-01</date><risdate>1996</risdate><volume>40</volume><issue>5</issue><spage>738</spage><epage>748</epage><pages>738-748</pages><issn>0031-3998</issn><eissn>1530-0447</eissn><coden>PEREBL</coden><abstract>The aim of this study was to produce a neonatal piglet model which, avoiding vessel ligation, exposed the whole animal to hypoxia and produced dose-dependent clinical encephalopathy and neuropathologic damage similar to that seen after birth asphyxia. Twenty-three piglets were halothane-anesthetized. Hypoxia was induced in 19 piglets by reducing the fractional concentration of inspired oxygen (FiO2) to the maximum concentration at which the EEG amplitude was below 7 microV (low amplitude) for 17-55 min. 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source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Journals@Ovid Complete; Alma/SFX Local Collection
subjects Animals
Biological and medical sciences
Brain - pathology
Brain - physiopathology
Delivery. Postpartum. Lactation
Disease Models, Animal
Disorders
Electroencephalography
Gynecology. Andrology. Obstetrics
Heart - physiopathology
Humans
Hypoxia - pathology
Hypoxia - physiopathology
Infant, Newborn
Kidney - pathology
Liver - pathology
Lung - pathology
Medical sciences
Swine
title A piglet survival model of posthypoxic encephalopathy
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