Effects of experimental ischemia on electrolytes of cortical cerebrospinal fluid and on brain water

✓ A procedure for perfusion over the cortical surfaces of the cerebral hemispheres of monkeys (Macaca mulatta) was used in combination with a procedure for producing sudden, temporary circulatory arrest in one hemisphere while the carotid circulation to the other hemisphere remained intact. The underlying disturbance in brain metabolism subsequent to circulatory arrest for 60 minutes was reflected in part by a decrease in the concentration of sodium and an elevation in the concentration of potassium in the cortical cerebrospinal fluid (CSF) on the ischemic side. The changes occurred at or within 30 minutes of the onset of circulatory arrest. The concentration of chloride in the cortical CSF on the ischemic side did not show significant differences from the control values. The ischemic brain exhibited as much as 18% swelling of cortical gray matter and 16% swelling of subcortical white matter at 5 hours after reestablishment of the carotid circulation. Vascular injury pursuant to ischemia was reflected in a significantly increased permeability to 131I-albumin entering the cortical CSF from the cerebral blood vessels. It is suggested that the CSF and vascular water are the sources of increased brain water.