Blood to Brain Sodium Transport and Interstitial Fluid Potassium Concentration during Early Focal Ischemia in the Rat

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Abstract
During partial ischemia, sodium and potassium ions exchange across the blood–brain barrier, resulting in a net increase in cations and brain edema. Since this exchange is likely mediated by specific transporters such as Na,K–ATPase in the capillary endothelium and because brain capillary Na,K–ATPase activity is stimulated by increased extracellular potassium in vitro, this study was designed to determine if the rate of blood to brain sodium transport is increased in ischemic tissue having an elevated interstitial fluid potassium concentration ([K]ISF) in vivo. Sprague-Dawley rats were studied between 2–3 h after occlusion of the right middle cerebral artery. To identify where cortical tissue with an elevated [K]ISF could be sampled for transport studies, the regional pattern of cerebral blood flow and [K]ISF was obtained in a group of 17 rats using hydrogen clearance and potassium-selective microelectrode techniques. We observed severely elevated [K]ISF (> 10 m M) when CBF was less than 20 ml 100 g−1 min−1 and mildly elevated levels at CBF between 20–45 ml 100 g−1 min−1. In a second group of seven rats, permeability-surface area products (PS products) for 22Na and [3H]α-aminoisobutyric acid ([3H]AIB) were determined in ischemic cortex with elevated [K]ISF and in nonischemic cortex. The PS products for AIB were similar in both tissues (2.2 ± 0.7 and 2.1 ± 0.4 μl/g/min) while the PS products for sodium was significantly increased in the ischemic tissue (1.5 ± 0.2 and 2.4 ± 1.1 μl/g/min). This study demonstrates that blood to brain sodium transport is increased in ischemic tissue at early times before the BBB is disrupted. Stimulation of the Na,K pumps in the capillary endothelium by elevated [K]ISF may mediate this effect.