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PubMed · 911225

Cerebral microembolization. I. Pathophysiological studies.

W M Vise·F Schuier·K A Hossmann·S Takagi·K J Zülch
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Abstract

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.

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AnimalsBlood GlucoseBlood-Brain BarrierBrain EdemaCatsCerebral CortexDisease Models, AnimalElectroencephalographyIntracranial Embolism and ThrombosisIntracranial PressureLactatesOxygenJournal Article

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W M Vise, F Schuier, K A Hossmann, S Takagi, K J Zülch. 1977. Cerebral microembolization. I. Pathophysiological studies.. https://doi.org/10.1001/archneur.1977.00500230030004

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