Stroke, Vol 18, 751-759, Copyright © 1987 by American Heart Association
W Young, ZH Rappaport, DJ Chalif and ES Flamm
Middle cerebral artery occlusions (MCAo) in rats produce infarcts in the
pyriform and frontoparietal cortex, extending into the lateral basal
ganglia and parasagittal cortex. We estimated tissue H2O concentrations
from wet and dry weight measurements and determined Na and K concentrations
by atomic absorption spectroscopy in these areas of rat brains. Tissue
samples were analyzed at 2, 4, and 24 hours after MCAo and sham MCAo,
compared with normal values measured in unoperated rats. In the pyriform
and frontoparietal areas, H2O concentrations increased to 34 and 7% greater
than normal by 2 hours, and 89 and 94% by 24 hours after MCAo. Na
concentrations rose in these areas to 73 and 37% greater than normal by 2
hours, and 281 and 330% by 24 hours. K concentrations did not change until
4 hours, but fell to 62 and 34% of normal in these areas by 24 hours. Such
large ion shifts indicate severe tissue destruction. In the parasagittal
cortex and basal ganglia areas, the ion and water changes were smaller and
did not become significant until 24 hours after MCAo. Rates of Na entry
into the infarct site were greatest at 0-2 hours, while the rates of K loss
peaked later, between 2 and 4 hours. The difference in Na influx and K
efflux resulted in net ion shifts that correlated highly with water entry,
yielding a correlation coefficient of 0.992 (p less than 0.001) and a slope
indicating that 1 ml of water entered the tissue with each 145 mumoles of
ions. These findings strongly suggest that net ion shifts cause the early
edema of regional brain ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Regional brain sodium, potassium, and water changes in the rat middle cerebral artery occlusion model of ischemia
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