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Howard S. Kirshner, MD; William F. Blank, Jr, MD; Ronald E. Myers, MD, PhD

Arch Neurol. 1976;33(2):84-90.

Abstract
• Seventeen rhesus monkeys underwent 20-minute episodes of hypoxia (mean Po₂' 18 to 28 mm Hg). In 14 animals that maintained mean blood pressures >60 mm Hg, increases in potassium concentration averaging >1 mEq/ liter were observed in the cortical subarachnoid fluid. These changes were reversible with oxygen administration and were usually not associated with morphologic evidence of brain injury. Cisterna magna fluid, sampled in five animals, showed smaller increases in potassium concentration (mean, 0.3 ± 0.4 mEq/ liter). The arteriovenous difference in potassium concentration was consistently positive, suggesting movement of potassium from blood to brain during hypoxia. The amount of potassium accumulation in the cortical subarachnoid fluid was closely related to the severity of the hypoxia. Threshold Po₂ levels, below which potassium changes occurred, were estimated at 29 mm Hg for the arterial blood and 20 mm Hg for the jugular venous blood. Massive potassium accumulations in the cortical subarachnoid fluid (>10 mEq/liter) developed in three animals that sustained severe arterial hypotension during hypoxia.

Author Affiliations
From the Laboratory of Perinatal Physiology, National Institute of Neurological Diseases and Stroke, Bethesda, Md.

Footnotes
Accepted for publication Feb 10, 1975.

Reprint requests to Laboratory of Perinatal Physiology, National Institute of Neurological Diseases and Stroke, Auburn Bldg, Room 106, Bethesda, MD 20014 (Dr Kirshner).

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