Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
1992-3-23
pubmed:abstractText
The effect of postischemic halothane anesthesia on locomotor activity and delayed neuronal injury in the hippocampal CA1 sector was examined in gerbils subjected to 5-min forebrain ischemia. Locomotor activity was assessed for 48 h after ischemia using an animal activity monitor, and CA1 injury was evaluated by counting the number of surviving neurons following 7 days of recirculation. Sham-treated animals exhibited a slight decrease of motor activity for about 1 day after surgery. Gerbils subjected to ischemia without postischemic halothane anesthesia developed significant motor hyperactivity (18 times higher than control activity) between 1.7 h and 6.7 h of recirculation. Surviving CA1 neurons in this group amounted to only 17% of those in the control animals. Postischemic halothane anesthesia during the initial 1.7 h of recirculation abolished subsequent motor hyperactivity and protected 84% of all CA1 neurons. Postischemic halothane anesthesia during 1.7 h-3.3 h of recirculation and 3.3-5 h of recirculation did not abolish motor hyperactivity except during the period of anesthesia, and did not protect hippocampal CA1 neurons (only 24% and 10% neuronal survival, respectively). These results demonstrate that the therapeutic window of halothane anesthesia for protection of hippocampal injury precedes the phase of locomotor hyperactivity, and that the appearance of the latter predicts delayed neuronal death.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-8993
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
563
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
33-8
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Therapeutic window of halothane anesthesia for reversal of delayed neuronal injury in gerbils: relationship to postischemic motor hyperactivity.
pubmed:affiliation
Max-Planck-Institute for Neurological Research, Department of Experimental Neurology, Cologne, F.R.G.
pubmed:publicationType
Journal Article