Abstract
1. The swelling of intact primate cerebral cortex perfused under isosmotic conditionsin vivo, like swelling of slices of mammalian cerebral cortex incubatedin vitro, is a linear function of the concentration of K+ in the extracellular fluid over the range 20–120 mM. 2. The simultaneous presence of the Cl− ion is required for the development of K+-dependent swelling of cerebral cortex under various experimental conditionsin vivo andin vitro. 3. The maintenance of previously established K+-dependent swelling of cerebral cortex bothin vitro andin vivo requires the relative concentrations of both K+ and Cl− in the extracellular fluid to remain constant. A reduction in the concentration of either ion is associated with an absolute loss of fluid of swelling of cerebral cortex. 4. The content of Cl− in cerebral cortex is a function of the magnitude of K+-dependent swelling even though the concentration of Cl− in the extracellular fluid is maintained constant. 5. The mechanism of swelling in primate cerebral cortex following cerebral circulatory arrest is discussed in the light of the experimental findings, as a model of the type of brain injury encountered in massive clinical stroke.
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