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(Stroke. 1997;28:206-210.)
© 1997 American Heart Association, Inc.

Articles

Extracellular Potassium in a Neocortical Core Area After Transient Focal Ischemia

Gunilla Gido, MSc; Tibor Kristian, PhD Bo K. Siesjo, MD, PhD

the Laboratory for Experimental Brain Research, Experimental Research Centre, University Hospital, Lund, Sweden, and the Institute of Neurobiology, Slovak Academy of Sciences, Kosice, Slovak Republic.

Correspondence to Gunilla Gido, Laboratory for Experimental Brain Research, Wallenberg Neurocenter, University Hospital, S-221 85, Lund, Sweden. E-mail gunilla.gido@eforsk.lu.se.

Background and Purpose Occlusion of the middle cerebral artery (MCAO) results in bioenergetic failure in the densely ischemic core areas. During reperfusion, transient recovery of the bioenergetic state is followed by secondary deterioration. In this study, we recorded the extracellular potassium concentrations in the cortical core during 2 hours of MCAO, as well as during recovery. One group of animals with recirculation periods of 6 to 8 hours was given the free radical spin trap -phenyl-N-tert-butyl nitrone (PBN).

Methods The experiments were performed on adult male Wistar rats (305 to 335 g). The right MCA was occluded by an intraluminal filament technique. For [K⁺]_e measurements a craniotomy was made over the right cortex, and an ion-sensitive microelectrode was lowered into the ischemic focus. Recording of [K⁺]_e was continued for 2 hours. After 48 hours of reperfusion, infarction size was estimated with 2,3,5-triphenyltetrazolium chloride.

Results During MCA occlusion, [K⁺]_e rose to 60 mmol/L. However, several animals showed transient (and partial) periods of repolarization accompanied by a decrease in [K⁺]_e. Immediately on reperfusion, the [K⁺]_e started to recover and reached baseline levels (2.5 mmol/L) within 3 to 5 minutes. During the first 6 hours of recovery, [K⁺]_e was stable at about 2.5 mmol/L, but after this period a moderate increase in the [K⁺]_e was observed. This was not observed in animals injected with PBN 1 hour after reperfusion.

Conclusions The data suggest that delayed cell membrane dysfunction, as reflected in a rise in [K⁺]_e, occurs after about 6 hours of reperfusion and that treatment with PBN in a single dose ameliorates or delays such deterioration of plasma membrane function.

Editorial Comment

Raymond C. Koehler, PhD, Guest Editor

The Johns Hopkins University Department of Anesthesiology and Critical Care Medicine Baltimore, Md

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