Source:http://linkedlifedata.com/resource/pubmed/id/12736390
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2003-7-25
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pubmed:abstractText |
The neuroprotective effect of hypothermia instituted after resuscitation from asphyxic cardiac arrest has not been studied in immature brain, particularly in a large animal model with recovery periods greater than 4 d. Moreover, protection from severe hypoxia seen with 3 h of hypothermia was reported to be lost when hypothermic duration was extended to 24 h in unsedated piglets, in contrast to the neuroprotection reported by 72 h of intrauterine head cooling in fetal sheep. Piglets (5-7 postnatal days) were subjected to asphyxic cardiac arrest followed by 24 h of either hypothermia (34 degrees C) or normothermia (38.5-39 degrees C). Comparisons were made with normothermic and hypothermic surgical sham animals without asphyxia. All of these groups were sedated, paralyzed, and mechanically ventilated for the first 24 h to prevent shivering and possible depletion of glucose stores. Hypothermia per se did not cause remarkable structural abnormalities. Ischemic damage was evaluated in putamen at 1 d of recovery without rewarming and at 11 d (10 d +/- SD after rewarming). Ischemic cytopathology affected 60 +/- 12% of neurons in putamen of normothermic animals compared with 9 +/- 6% in hypothermic animals at 1 d of recovery without rewarming. At 11 d of recovery from hypoxia-ischemia, the density of viable neurons (neuron profiles/mm2) in putamen was markedly reduced in normothermic animals (81 +/- 40) compared with hypothermic animals (287 +/- 22), which was the same as in sham normothermic (271 +/- 21), sham hypothermic (288 +/- 46) and naïve animals (307 +/- 51). These data demonstrate that 24 h of hypothermia at 34 degrees C with sedation and muscle relaxation after asphyxic cardiac arrest prevents necrotic striatal neuronal cell death in immature brain before rewarming, and that the effect is sustained at 11 d after injury without deleterious side effects.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0031-3998
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
54
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
253-62
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12736390-Acute Disease,
pubmed-meshheading:12736390-Animals,
pubmed-meshheading:12736390-Asphyxia,
pubmed-meshheading:12736390-Behavior, Animal,
pubmed-meshheading:12736390-Body Temperature,
pubmed-meshheading:12736390-Corpus Striatum,
pubmed-meshheading:12736390-Electroencephalography,
pubmed-meshheading:12736390-Heart Arrest,
pubmed-meshheading:12736390-Hot Temperature,
pubmed-meshheading:12736390-Hypothermia, Induced,
pubmed-meshheading:12736390-Male,
pubmed-meshheading:12736390-Necrosis,
pubmed-meshheading:12736390-Rectum,
pubmed-meshheading:12736390-Swine,
pubmed-meshheading:12736390-Weight Gain
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pubmed:year |
2003
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pubmed:articleTitle |
Hypothermia for 24 hours after asphyxic cardiac arrest in piglets provides striatal neuroprotection that is sustained 10 days after rewarming.
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pubmed:affiliation |
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Hospital, Blalock 1404, 600 N. Wolfe Street, Baltimore, MD 21287 U.S.A. rkoehler@jhmi.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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