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Bimodal treatment with nimodipine and low‐molecular‐weight dextran for focal cerebral ischemia in the rat
Author(s) -
Salgado Antonio V.,
Jones Stephen C.,
Furlan Anthony J.,
Korfali Ender,
Marshall Sam A.,
Little John R.
Publication year - 1989
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410260506
Subject(s) - nimodipine , cerebral blood flow , hematocrit , medicine , anesthesia , middle cerebral artery , ischemia , blood flow , anterior cerebral artery , common carotid artery , dextran , carotid arteries , chemistry , biochemistry , calcium
Abstract We compared the effects of intravenous treatment with combined low‐molecular‐weight dextran and nimodipine (n = 9), or placebo (n = 10), on local cerebral blood flow after occlusion of the left middle cerebral and common carotid artery in the rat. Treatment for a total of 4 hours with low‐molecular‐weight dextran (5 mg/kg/min) and nimodipine (0.25 μg/kg/min) produced a decrease in hematocrit from 46 ± 1 to 33 ± 1% at the end of the study and a statistically significant increase in local cerebral blood flow, when compared to the control group, in 6 regions of interest: the territories of the right middle ( p = 0.01), right anterior ( p = 0.007), and left anterior cerebral arteries ( p = 0.001) the superior ( p = 0.03) and inferior border zone ( p = 0.003); and white matter in the right hemisphere ( p = 0.04). The ischemic volume, defined as brain volume with a cerebral blood flow of less than the critical level of 25 ml/min/100 gm was determined as a percentage of total brain volume for the control and treatment groups. The group treated with lowmolecular‐weight dextran and nimodipine showed a 31% decrease in ischemic volume ( p = 0.03). These results indicate that a bimodal approach with low‐molecular‐weight dextran and nimodipine can be safely used in a model of acute stroke and has a beneficial effect on local cerebral blood flow and ischemic volume when compared with control subjects. After 4 hours, the potential exists that this treatment is therapeutic, assuming that the ischemic volume progresses to infarction.