EXTRACELLULAR POTASSIUM IN A NEOCORTICAL CORE AREA AFTER TRANSIENT FOCAL ISCHEMIA

Background and Purpose Occlusion of the middle cerebral artery (MCAO) results in bioenergetic failure in the densely ischemic core areas. Du ring reperfusion, transient recovery of the bioenergetic state is foll owed by secondary deterioration. In this study, we recorded the extrac ellular potassium concentrations in the cortical core during 2 hours o f MCAO, as well as during recovery. One group of animals with recircul ation periods of 6 to 8 hours was given the free radical spin trap alp ha-phenyl-N-tert-butyl nitrone (PEN). Methods The experiments were per formed on adult male Wistar rats (305 to 335 g). The right MCA was occ luded by an intraluminal filament technique. For [K+](e) measurements a craniotomy was made over the right cortex, and an ion-sensitive micr oelectrode was lowered into the ischemic focus. Recording of [K+](e) w as continued for 2 hours. After 48 hours of reperfusion, infarction si ze was estimated with 2,3,5-triphenyltetrazolium chloride. Results Dur ing MCA occlusion, [K+](e) rose to approximate to 60 mmol/L. However, several animals showed transient (and partial) periods of repolarizati on accompanied by a decrease in [K+](e). Immediately on reperfusion, t he [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 incre ase in the [K+](e) was observed. This was not observed in animals inje cted with PEN 1 hour after reperfusion. Conclusions The data suggest t hat delayed cell membrane dysfunction, as reflected in a rise in [K+]( e), occurs after about 6 hours of reperfusion and that treatment with PEN in a single dose ameliorates or delays such deterioration of plasm a membrane function.