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Clinical Neurosurgery 1981-Jul

Treatment of acute focal cerebral ischemia with dimethyl sulfoxide.

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J R Little
A Cook
R P Lesser

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The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 +/- 10 ml/100 g/minute in the untreated group and 45 +/- 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled erythrocytes in the right sylvian region. The period of erythrocyte transit before occlusion was 10 +/- 1 seconds in the untreated group and 10 +/- 2 seconds in the treated group. After 6 hours of occlusion, the erythrocyte transit time was 18 +/- 3 seconds in the untreated group and 19 +/- 3 seconds in the treated group. Increasing delay in erythrocyte transit during the 6-hour occlusion period was seen in 5 untreated cats and 6 treated cats and was thought to represent a progressive increase in microvascular resistance. The complete washout of erythrocytes indicated the absence of microcirculatory obstruction. Electroencephalography (EEG) showed a reduced amplitude of activity in the right cerebral hemisphere after occlusion in cats with an rCBF consistently below 18 ml/100 g/minute. No significant EEG differences were found between the untreated and treated groups. Treatment with DMSO failed to modify the developing ischemia edema, neuronal alterations, or the changes in blood-brain barrier permeability to Evans blue dye and fluorescein. In this study DMSO was ineffective in preventing ischemic damage or acted when irreversible injury had already taken place.

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