Cerebral microembolization. I. Pathophysiological studies.
Unilateral embolization of the brain was performed in cats by intracarotid injection of 10.5 million carbonized microspheres (15 +/- 5 mu). Intracranial pressure increased from 6.1 +/- 1.5 to 14 +/- 2.3 mm Hg within two minutes and continued to rise more slowly to 24 +/- 18.3 mm Hg within four hours. Embolization caused a nonhomogenous distribution of microflow, but initially had no effect on global cerebral blood flow, nor on cortical oxygen tension. Yet, a functional suppression of cortical electrical and metabolic activity occurred. The ipsilateral EEG flattened irreversibly after 15 seconds; the contralateral EEG was transiently suppressed shortly thereafter. Arteriovenous difference of oxygen fell from 10.5 +/- 0.7 to 5.3 +/- 0.6 vol%, and the arteriovenous difference of glucose fell from 11.7 +/- 3.9 to 2.6 +/- 2.1 mg/100 ml as a consequence of reduced oxygen and glucose extraction. Subsequently, severe vasogenic brain edema, secondary ischemia, and severe functional suppression developed between two and four hours.
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001812:Blood-Brain Barrier; D001929:Brain Edema / Q000209:etiology; D002415:Cats; D002540:Cerebral Cortex / Q000098:blood supply; D004195:Disease Models, Animal; D004569:Electroencephalography; D002542:Intracranial Embolism and Thrombosis / Q000150:complications / Q000378:metabolism / Q000503:physiopathology*; D007427:Intracranial Pressure; D007773:Lactates / Q000097:blood; D010100:Oxygen / Q000097:blood
D001786:Blood Glucose; D007773:Lactates; D010100:Oxygen