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Cerebral ischemia was produced in gerbils by ligation of the right common carotid artery and the resulting clinical manifestations and pathological alterations, along with electroencephalographic findings, were followed from 30 minutes to 24 hours. Protein synthesis was evaluated with brain slices in vitro and subsequent cellular and subcellular fractionations. One group of animals developed clinical signs of cerebral ischemia and stroke very rapidly and often died within 12 hours. In these animals cerebral infarction was diffuse in the right side of brain within a few hours post-operatively and there was persistent suppression in the electroencephalographic recordings. Amino acid incorporation into protein of subcellular fractions was decreased to 50% of the opposite side at 30 minutes and further declined to less than 10% in 8 to 10 hours. Another group of animals survived to 24 hours in spite of severe neurological manifestations, and protein synthesis was about 15% of the control side at 24 hours. The suppression of protein synthesis was observed both in the neuronal and neurologlial fractions indicating similar vulnerability of these cellular elements toward cerebral ischemia as shown with cerebral anoxia in the past. It was emphasized that the correlation of clinical manifestations and biochemical data is very important to extract meaningful information from biochemical investigations in this model.

Experimental stroke in gerbils: correlation of clinical, pathological and electroencephalographic findings and protein synthesis.