Effect of sedative dose of propofol on neuronal damage after transient forebrain ischemia in Mongolian gerbils
The Korean Journal of Physiology and Pharmacology
;
: 73-79, 2000.
Article
in English
| WPRIM
| ID: wpr-728336
ABSTRACT
This study investigated whether propofol, an intravenous, non-barbiturate anesthetic, could reduce brain damage following global forebrain ischemia. Transient global ischemia was induced in gerbils by occlusion of bilateral carotid arteries for 3 min. Propofol (50 mg/kg) was administered intraperitoneally 30 min before, immediately after, and at 1 h, 2 h, 6 h after occlusion. Thereafter, propofol was administered twice daily for three days. Treated animals were processed in parallel with ischemic animals receiving 10% intralipid as a vehicle or with sham-operated controls. In histologic findings, counts of viable neurons were made in the pyramidal cell layer of the hippocampal CA1 area 4 days after ischemia. The number of viable neurons in the pyramidal cell layer of CA1 area was similar in animals treated with a vehicle or a subanesthetic dose of propofol. In terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end-labeling (TUNEL) assay, semiquantitative analysis of dark-brown neuronal cells was made in the hippocampal CA1 area. There was no significant difference in the degree of TUNEL staining in the hippocampal CA1 area between vehicle-treated and propofol-treated animals. These results show that subanesthetic dose of propofol does not reduce delayed neuronal cell death following transient global ischemia in Mongolian gerbils.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Brain
/
Carotid Arteries
/
Propofol
/
Gerbillinae
/
Prosencephalon
/
Cell Death
/
Pyramidal Cells
/
In Situ Nick-End Labeling
/
DNA Nucleotidylexotransferase
/
Ischemia
Limits:
Animals
Language:
English
Journal:
The Korean Journal of Physiology and Pharmacology
Year:
2000
Type:
Article
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