Abstract |
Our studies showed that in an appropriate dose, nimodipine increased local cerebral blood flow with no corresponding increase in local metabolism. Nimodipine treatment given before experimental ischemic insult, resulting from either vascular occlusion or intracranial hemorrhage or after subarachnoid hemorrhage, maintained or improved blood flow and minimized the severity of subsequent brain damage. Lack of benefit from nimodipine treatment after the insult may occur because the inexorable progression of events leading to ischemic neuronal damage, once initiated, cannot be arrested. On the other hand, pharmacokinetic factors may be important, and post-treatment efficacy may depend on administration protocols that achieve an adequate concentration in ischemic tissue sufficiently soon after an insult. Our findings are compatible with the benefit of nimodipine being due to an improvement in blood flow that reduces the severity of ischemia. However, they do not exclude the possibility that treatment may minimize the accumulation of calcium in damaged cells as a result of "cytoprotective" effects.
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Authors | G Teasdale, A D Mendelow, D I Graham, A M Harper, J McCulloch |
Journal | Stroke
(Stroke)
Vol. 21
Issue 12 Suppl
Pg. IV123-5
(Dec 1990)
ISSN: 0039-2499 [Print] United States |
PMID | 2260136
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)
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Chemical References |
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Topics |
- Animals
- Cerebral Hemorrhage
(drug therapy)
- Disease Models, Animal
- Humans
- Ischemic Attack, Transient
(drug therapy)
- Nimodipine
(therapeutic use)
- Subarachnoid Hemorrhage
(drug therapy)
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