ROLE OF K-FLOW IN THE RAT - EFFECT OF GLIBENCLAMIDE AND OUABAIN( IN REGULATING HYPOXIC CEREBRAL BLOOD)

We assessed the role of extracellular potassium ([K+](e)) on the incre ase in cerebral blood flow (CBF) during hypoxia, and we tested whether it was affected by glibenclamide or ouabain. Cortical CBF was measure d using the hydrogen clearance technique in enflurane-anesthetized rat s, and local [K+](e) was measured with K+ microelectrodes adjacent to the hydrogen electrode. Eucapnic hypoxia (arterial P-O2 similar to 35- 40 Torr) increased CBF twofold and caused a modest rise in [K+](e) (fr om 2.9 +/- 0.2 to 3.7 +/- 0.2 mM; mean arterial blood pressure, ABP, 8 6 +/- 5 mmHg). If ABP fell <70 mmHg during hypoxia, no increase in CBF was seen, whereas [K+](e) increased to >20 mM. Glibenclamide (10-100 mu M intracortically) attenuated [K+](e) and CBF during hypoxia (ABP s imilar to 75 mmHg, P < 0.01). Ouabain (20-1,000 mu M) increased [K+](e ); however, it did not remove the hypoxic-induced rise in [K+](e). We conclude that glibenclamide-sensitive potassium channels contribute to the accumulation of [K+](e) during hypoxia, although an increase in C BF during hypoxia can occur without a marked rise in [K+](e). Furtherm ore, if ABP falls below the lower limit of autoregulation during hypox ia, there is no increase in CBF, yet there is a large increase in [K+] (e).