Abstract | PURPOSE: METHODS: The endovascular perforation model of SAH was produced and animals were randomly assigned to sham-operated rats, saline-treated (vehicle), and 10 mg/kg of SOV-treated SAH rats. Drugs were injected intraperitoneally immediately after SAH induction. Neurological score and brain water content (BWC) were assessed at 24 h after SAH. Cell injury was studied by terminal deoxynucleotidyl transferase-mediated uridine 5'-triphosphate-biotin nick end-labeling (TUNEL) at 24 h after SAH. RESULTS: Severity of SAH and mortality in SOV-treated rats was similar to that of the saline group. SOV significantly decreased BWC and improved neurological score at 24 h after SAH compared with the saline group. SOV decreased TUNEL-positive cells at 24 h after SAH compared with the saline group. CONCLUSIONS:
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Authors | Yu Hasegawa, Hidenori Suzuki, Prativa Sherchan, Yan Zhan, Kamil Duris, John H Zhang |
Journal | Acta neurochirurgica. Supplement
(Acta Neurochir Suppl)
Vol. 110
Issue Pt 1
Pg. 67-70
( 2011)
ISSN: 0065-1419 [Print] Austria |
PMID | 21116917
(Publication Type: Journal Article, Research Support, N.I.H., Extramural)
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Chemical References |
- Vanadates
- Protein Tyrosine Phosphatases
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Topics |
- Animals
- Brain Edema
(drug therapy, etiology)
- Brain Injuries
(drug therapy, enzymology, etiology, mortality)
- Cell Death
(drug effects)
- Disease Models, Animal
- In Situ Nick-End Labeling
(methods)
- Male
- Neurologic Examination
- Protein Tyrosine Phosphatases
(metabolism)
- Rats
- Rats, Sprague-Dawley
- Severity of Illness Index
- Subarachnoid Hemorrhage
(complications)
- Time Factors
- Vanadates
(therapeutic use)
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