Metabolic, ionic, and electrical responses of gerbil brain to ischemia

The effecs of short- or long-term complete cerebral ischemia were studied in the gerbil brain using a multiparameter monitoring system. Metabolic (NADH redox state) and hemodynamic responses were monitored by surface fluorometry-reflectomery. Ionic activities (K⁺ and pH) were measured by surface macroelectrodes. Electrical activity was evaluated by monitoring the general electrocorticogram (ECoG) as well as local DC steady potential (two sites). Two groups of gerbils were studied to compare the effects of 4-5 min occlusions with those of 30 min complete ischemia. During bilateral carotid artery occlusion the cortex is exposed to complete ischemia resulting in the complete depletion of O₂ with attendant maximal reduction of NADH. Extracellular K⁺ began to increase as soon as energy reserves were decreased with a time course suggesting two different kinetic areas. Surface pH decreased very shortly after the occlusion. During the recovery phase, NADH was reoxidized soon after recirculation, whereas the pH and K⁺ recovery showed a short delay, ECoG did not recover even when all other parameters reached base-line levels. The recovery of all the measured parameters was correlated to the duration of the ischemic insult; i.e. the recovery from 30 min of ischemia took significantly longer than after 5 min of ischemia. We conclude that pH recovery depends on recirculation and adequate O₂ supply to the tissue, whereas K⁺ recovery required not only an adequate O₂ supply but also the integrity of the adenosine triphosphate system.