Effects of phenobarbital in cerebral ischemia. Part II: restitution of cerebral energy state, as well as of glycolytic metabolites, citric acid cycle intermediates and associated amino acids after pronounced incomplete ischemia.

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Abstract
Recovery of cerebral energy metabolism, following 15 or 30 min of pronounced, incomplete ischemia, was studied after 90 min of recirculation in rats that were either anesthetized with 70% N2O or 150 mg.cntdot.kg-1 of phenobarbital. In all animals arterial blood pressure, PO2 [partial pressure of O2] and PCO2 were close to normal during recirculation. In N2O-anesthetized animals kept ischemic for 30 min, but not in those given phenobarbital, a gradual rise in intracranial cerebrospinal fluid (CSF) pressure (to about 20-25 mm Hg) occurred during the last 20-30 min of recirculation. Following 15 min of ischemia, all phenobarbital-anesthetized animals and 20 out of 24 animals anesthetized with 70% N2O, showed extensive restitution of cerebral energy metabolism, including normalization of phosphocreatine concentration, return of adenylate energy charge to about 99% of control, and disappearance of virtually all of the lactate accumulated during the ischemia. A near-normal mitochondrial metabolism apparently returned. Following 30 min of ischemia in phenobarbital-anesthetized animals, a similar degree of recovery was observed. No animal maintained on 70% N2O showed such signs of metabolic recovery. Complete ischemia is followed by a significantly better recovery of cerebral energy metabolism than is a corresponding period of incomplete ischemia. Phenobarbital protects under conditions of incomplete ischemia even when it does not prevent energy depletion from rapidly occurring during ischemia.