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Experimental cerebral ischemia produces platelet aggregates

Research Center in Cerebrovascular Disease, Department of Neurology (Drs. Dougherty and Levy), and the Division of Hematology, Department of Medicine (Dr. Weksler), Cornell University Medical College, New York, NY.

Address correspondence and reprint requests to Dr. Dougherty, Department of Neurology, Cornell University Medical College, 1300 Y ork Avenue, New York, NY 10021.

Human studies indicate that transient platelet abnormalities accompany acute cerebral ischemia. Although these abnormalities may precipitate the ischemic process, ischemia could also alter platelet function. Platelets were therefore studied in gerbils subjected to 1 hour of unilateral carotid artery occlusion. Venous blood from five clinically affected gerbils contained more aggregated platelets (37.8% ± 6.4) than did blood from eight unaffected animals (11.1% ± 3 .0; p <0.01). Platelets labeled with 3H-serotonin were increased in ishcemic brain; the ratio of radioactivity in the ipsilateral versus contralateral hemisphere was greater in eight dected (1.09 f 0.03) than in 19 unaffected (1.00 ± 0.01; p <0.02) animals. The radioactive serotonin was located predominantly within blood vessels. Cerebral ischemia thus stimulated the formation of platelet aggregates, a response which could contribute to the ischemic process.

Accepted for publication April 24, 1979.

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