Cerebral hypothermia is not neuroprotective when started after postischemic seizures in fetal sheep

Prolonged cerebral hypothermia is neuroprotective if started within a few hours of hypoxia-ischemia. However, delayed seizure activity is one of the major clinical indicators of an adverse prognosis after perinatal asphyxia. The aim of this study was to determine whether head cooling delayed until a...

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Veröffentlicht in:Pediatric research 1999-09, Vol.46 (3), p.274-280
Hauptverfasser: GUNN, A. J, BENNET, L, GUNNING, M. I, GLUCKMAN, P. D, GUNN, T. R
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container_start_page 274
container_title Pediatric research
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creator GUNN, A. J
BENNET, L
GUNNING, M. I
GLUCKMAN, P. D
GUNN, T. R
description Prolonged cerebral hypothermia is neuroprotective if started within a few hours of hypoxia-ischemia. However, delayed seizure activity is one of the major clinical indicators of an adverse prognosis after perinatal asphyxia. The aim of this study was to determine whether head cooling delayed until after the onset of postasphyxial seizures may still be neuroprotective. Unanesthetized near-term fetal sheep in utero received 30 min of cerebral ischemia induced by bilateral carotid artery occlusion. Eight and one-half hours later, they received either cooling (n = 5) or sham cooling (n = 13) until 72 h after the insult. Intrauterine cooling, induced by circulating cold water through a coil around the fetal head, was titrated to reduce fetal extradural temperature from 39.4+/-0.1 degrees C to between 30 and 33 degrees C. Cerebral ischemia led to the delayed development of intense epileptiform activity from 6 to 8 h postinsult, followed by a marked secondary rise in cortical impedance (a measure of cytotoxic edema) and in carotid blood flow. Cerebral cooling markedly attenuated the secondary rise in impedance and reduced carotid blood flow (p < 0.001). After 5 d recovery, there was no significant difference in loss of parietal EEG activity relative to baseline in the hypothermia compared with the control group (-12.5+/-1.4 versus -15.2+/-1.2 dB, mean +/- SEM, NS) or in parasagittal cortical neuronal loss (82+/-9 versus 90+/-5%, NS). In conclusion, delayed prolonged head cooling begun after the onset of postischemic seizures was not neuroprotective. These data highlight the importance of intervention in the latent phase, after reperfusion but before the onset of secondary injury.
doi_str_mv 10.1203/00006450-199909000-00005
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Intrauterine cooling, induced by circulating cold water through a coil around the fetal head, was titrated to reduce fetal extradural temperature from 39.4+/-0.1 degrees C to between 30 and 33 degrees C. Cerebral ischemia led to the delayed development of intense epileptiform activity from 6 to 8 h postinsult, followed by a marked secondary rise in cortical impedance (a measure of cytotoxic edema) and in carotid blood flow. Cerebral cooling markedly attenuated the secondary rise in impedance and reduced carotid blood flow (p &lt; 0.001). After 5 d recovery, there was no significant difference in loss of parietal EEG activity relative to baseline in the hypothermia compared with the control group (-12.5+/-1.4 versus -15.2+/-1.2 dB, mean +/- SEM, NS) or in parasagittal cortical neuronal loss (82+/-9 versus 90+/-5%, NS). In conclusion, delayed prolonged head cooling begun after the onset of postischemic seizures was not neuroprotective. 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Sudden death</subject><subject>Female</subject><subject>Fetal Hypoxia</subject><subject>Fetus - blood supply</subject><subject>Fetus - physiopathology</subject><subject>Hypothermia, Induced</subject><subject>Intensive care medicine</subject><subject>Medical sciences</subject><subject>Pregnancy</subject><subject>Seizures - etiology</subject><subject>Seizures - prevention &amp; control</subject><subject>Sheep</subject><subject>Time Factors</subject><issn>0031-3998</issn><issn>1530-0447</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkEtLxDAQgIMo7rr6FyQH8VbNs2mOsvgCwYueS5pOaaQvk1TRX2_WXR9zGWb45sGHEKbkgjLCL0mKXEiSUa010anKNi25h5ZU8lQIofbRkhBOM651sUBHIbwQQoUsxCFaUCIUJ4IukV2Dh8qbDrcf0xhb8L0z2AU8jBEPMPtx8mMEG90b4PcWBhyi8RFqbJoIHk9jiC7YFnpncQD3OXsI2A24gZiWhhZgOkYHjekCnOzyCj3fXD-t77KHx9v79dVDZrkmMasl1IwrxQuWG6u0qripmClsLavG5FY1NKdasJoZy2qpiVWskAaIzqmoaspX6Hy7N738OkOIZZ9eg64zA4xzKFVSVBRKJ7DYgtaPIXhoysm73viPkpJyI7j8EVz-Cv5uyTR6ursxVz3U_wa3RhNwtgNMsKZrvBmsC3-czvNca_4FyXiEtA</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>GUNN, A. 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subjects Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy
Animals
Biological and medical sciences
Brain Ischemia - complications
Emergency and intensive care: neonates and children. Prematurity. Sudden death
Female
Fetal Hypoxia
Fetus - blood supply
Fetus - physiopathology
Hypothermia, Induced
Intensive care medicine
Medical sciences
Pregnancy
Seizures - etiology
Seizures - prevention & control
Sheep
Time Factors
title Cerebral hypothermia is not neuroprotective when started after postischemic seizures in fetal sheep
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