Abstract | OBJECTIVE: METHODS: Experimental SAH was performed in rabbits by injecting autologous blood into the cisterna magna. Intravenous injections of cromakalim or vehicle were administered twice daily with the first injection administered 1 hour after induction of SAH. Animals were killed by perfusion-fixation 48 hours after SAH. Basilar arteries were removed and sectioned, and the luminal cross-sectional areas were measured. RESULTS: Experimental SAH induced cerebral vasospasm in untreated and vehicle-treated animals. Cromakalim attenuated cerebral vasospasm in a dose-dependent manner. This effect achieved statistical significance at doses of 0.1 and 0.3 mg/kg. CONCLUSION: These results support the concept that targeting vascular K+ channels can be of benefit in preventing the development of cerebral vasospasm. The findings also indicate that cromakalim represents a potential therapeutic agent for the treatment of cerebrovascular pathophysiology after SAH.
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Authors | A L Kwan, C L Lin, H Yanamoto, S L Howng, N F Kassell, K S Lee |
Journal | Neurosurgery
(Neurosurgery)
Vol. 42
Issue 2
Pg. 347-50; discussion 350-1
(Feb 1998)
ISSN: 0148-396X [Print] United States |
PMID | 9482186
(Publication Type: Journal Article, Research Support, U.S. Gov't, P.H.S.)
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Chemical References |
- Potassium Channels
- Cromakalim
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Topics |
- Animals
- Basilar Artery
(drug effects, pathology)
- Cromakalim
(administration & dosage, therapeutic use)
- Dose-Response Relationship, Drug
- Injections, Intravenous
- Ischemic Attack, Transient
(drug therapy, etiology, pathology)
- Male
- Potassium Channels
(agonists)
- Rabbits
- Subarachnoid Hemorrhage
(complications)
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