BRAIN CALCIUM-METABOLISM IN HYPOGLYCEMIC COMA

The present experiments were designed to provide information on brain calcium metabolism during hypoglycemic coma. We specifically wished to evaluate changes in extracellular calcium concentration (Ca2+e) durin g prolonged hypoglycemic coma and recovery and to assess whether Ca2+e falls to similar values during hypoglycemia and ischemia. To that end , Ca2+e and K+e in neocortical tissue were recorded by ion-sensitive m icroelectrodes during hypoglycemic coma of 30 min duration and during 15 min of recovery. Cardiac arrest ischemia was induced either at the end of the period of hypoglycemia or after 15 min of recovery. Hypogly cemic coma, as reflected by a DC potential shift and by cellular relea se of K+, was accompanied by a sustained decrease in Ca2+e from approx imately 1.2 to approximately 0.02 mM, i.e., to approximately 1% of con trol. Infusion of glucose was followed by a biphasic recovery of Ca2+e , starting within 2 min of infusion. During the first phase, completed within the initial 3-4 min. Ca2+e rose to about 25% of control. Durin g the second phase, Ca2+e slowly increased toward normal within 25-30 min. Ischemia, when induced at the end of the period of hypoglycemia, was accompanied by a rise in Ca2+e to about 0.1 mM, i.e., about 10% of control. A similar value was recorded when ischemia was induced after 15 min of recovery following a 30-min hypoglycemic coma. Although the present results do not give information on Ca2+i during hypoglycemic coma, it is tempting to conclude that partial preservation of the nucl eoside triphosphate stores, and absence of acidosis, allow some bindin g and sequestration of the calcium entering the cell. Such binding and sequestration may explain the pronounced biphasic nature of the recov ery curves for Ca2+e. Thus, if one assumes that the rapid increase in Ca2+e represents extrusion of available ''free'' intracellular Ca2+, o ne can envisage that the slow phase of recovery represents calcium tha t is slowly extruded following its release from the binding and seques tration stores.