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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
1993-6-15
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pubmed:abstractText |
During brain ischemia temperature spontaneously declines. In animal experiments this decline is frequently prevented by stabilizing the temperature at the pre-ischemic level, using an external heat source. The present study examines whether this procedure influences the severity of ischemic injury. Wistar rats were submitted to 30-min four-vessel occlusion followed by 7 days recirculation. During ischemia and the 1st h of recirculation various systemic and electrophysiological variables were recorded. Seven days after the ischemia brains were perfusion-fixed for light microscopical examination. Three brain temperature profiles were compared: spontaneous decline of brain temperature during ischemia from 36 degrees to 31 degrees C (spontaneous hypothermia; n = 5); constant brain temperature of 30 degrees C induced by selective head cooling (induced hypothermia; n = 5); and constant brain temperature of 36 degrees C induced by selective head heating (normothermia; n = 5). Core temperature was maintained constant at 37 degrees C in all groups. In spontaneous hypothermia, 19% of CA1 neurons survived after 30-min ischemia. Induced hypothermia significantly increased this percentage to 69% (P < 0.05); maintenance of brain temperature at normothermia decreased neuronal survival to 1%. Normothermia also led to morphological injury outside the vulnerable regions, an increase in mortality, marked loss of body weight and a prolongation of the electroencephalographic suppression. These findings demonstrate that stabilizing brain temperature at a constant normothermic level by an external heart source introduces an aggravating pathological element that may interfere in an unpredictable way with the manifestation or treatment of ischemic injury.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:status |
MEDLINE
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pubmed:issn |
0001-6322
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
85
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
488-94
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8493858-Animals,
pubmed-meshheading:8493858-Blood Gas Analysis,
pubmed-meshheading:8493858-Blood Pressure,
pubmed-meshheading:8493858-Body Temperature,
pubmed-meshheading:8493858-Body Weight,
pubmed-meshheading:8493858-Brain,
pubmed-meshheading:8493858-Brain Injuries,
pubmed-meshheading:8493858-Brain Ischemia,
pubmed-meshheading:8493858-Carotid Arteries,
pubmed-meshheading:8493858-Electroencephalography,
pubmed-meshheading:8493858-Hot Temperature,
pubmed-meshheading:8493858-Male,
pubmed-meshheading:8493858-Prosencephalon,
pubmed-meshheading:8493858-Rats,
pubmed-meshheading:8493858-Rats, Wistar,
pubmed-meshheading:8493858-Tissue Fixation
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pubmed:year |
1993
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pubmed:articleTitle |
Heating of the brain to maintain normothermia during ischemia aggravates brain injury in the rat.
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pubmed:affiliation |
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Köln, Germany.
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pubmed:publicationType |
Journal Article
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