Brain potassium ion homeostasis, anoxia, and metabolic inhibition in turtles and rats.

Microelectrode measurements of tissue oxygen tension (PtO2) and extracellular potassium ion concentration ([K+]o) and dual wavelength spectrophotometric measurements of the reduction/oxidation state of cytochrome aa3 were used to compare the resistance of turtle and rat brain to anoxia in vivo. In both species, respiration with 100% N2 resulted in a decrease of tissue oxygen tension to near 0 mmHg and reduction of cytochrome aa3. However, N2 respiration resulted in only moderate elevation of [K+]o in turtle bran while [K+]o in rat brain was elevated to levels greater than 50 mM. In addition, N2 respiration in turtles had no effect on the rate of recovery of [K+]o, which was elevated by direct electrical stimulation of the brain. Electrocorticographic activity (ECoG) of the turtle brain was only moderately depressed during N2 respiration for up to 4 h whereas the ECoG of rat brain became isoelectric within 1 min. Inhibition of glycolysis with iodoacetate (IAA) resulted in rapid elevation of [K+]o in turtle brain during anoxia, but IAA had little effect on [K+]o during normoxia. These results indicate that the remarkable resistance of the diving turtle to anoxia does not result from continued provision of oxygen to the brain either by redistribution of systemic blood flow or from blood O2 storage. In addition, the turtle brain does not rely on cellular stores of high-energy compounds for maintenance of ionic homeostasis. We conclude that potassium ion homeostasis in the anoxic turtle brain must result from increased glycolytic ATP production and from decreased energy utilization.