Abstract
The relationship between brain tissue calcium content and postischemic electrophysiological and metabolic recovery was investigated in 18 adult normothermic cats, 12 of which were submitted to 1 h of complete ischemia and 3 h of recirculation. Six animals served as controls. Functional recovery was estimated by recording the electrocorticogram (ECoG) and evoked potentials, and biochemical recovery by regional evaluation of ATP, glucose, and pH in intact brain sections. One group of animals was treated with the calcium antagonist flunarizine (0.1 mg/kg i. v., followed by continuous i. v. infusion of 0.1 mg/kg/h during the recirculation phase); another group did not receive this treatment. Evoked potentials in all six untreated animals (and in four also, spontaneous ECoG activity) returned after ischemia. In the animals with ECoG activity, biochemical recovery was homogeneous, as indicated by a return toward normal of regional tissue ATP and glucose content. In one animal without ECoG activity, several small regions were present in which energy metabolism was impaired. In regions with biochemical recovery, brain tissue calcium significantly increased by ∼35% (controls, 0.330 ± 0.045; ischemia, 0.447 ± 0.194 μg/mg protein; means ± SD). Changes were accompanied by a parallel increase in sodium (controls, 7.72 ± 1.92; ischemia, 10.50 ± 2.47 μg/mg protein), a slight decrease of potassium (controls, 29.52 ± 0.85; ischemia, 27.66 ± 2.30 μg/mg protein), and an increase of tissue pH (controls, 7.10 ± 0.096; ischemia, 7.307 ± 0.083). In regions without biochemical recovery, pH fell to 6.288 ± 0.157, and calcium content was 0.602 ± 0.235, sodium content 11.70 ± 4.60, and potassium content 23.00 ± 3.91 μg/mg protein. Treatment with the calcium antagonist flunarizine did not reduce tissue calcium content, nor did it improve functional or metabolic recovery after ischemia: three of six treated animals exhibited ECoG activity, one showed only evoked potentials, and two showed no recovery at all. It is concluded that postischemic accumulation of calcium in brain tissue cannot be prevented by the calcium antagonist flunarizine. However, the observed increase of calcium did not interfere with the early postischemic electrophysiological and biochemical recovery. Its pathophysiological importance, therefore, may be associated with more delayed postischemic disturbances.