The Effect of Intravenous or Subarachnoid Lidocaine on Glutamate Accumulation During Transient Forebrain Ischemia in Rats

Abstract

We studied whether IV or subarachnoid (SA) lidocaine would influence the increase in extracellular glutamate concentration in the hippocampal CA1 and the cerebral cortex during transient forebrain ischemia in rats by using the dialysis electrode method. Fifty-four Sprague-Dawley rats were assigned to one of six treatment groups: IV lidocaine 5 mg/kg, IV lidocaine 10 mg/kg, IV 0.9% saline 0.5 mL/kg, SA lidocaine 5 mg/kg, SA lidocaine 10 mg/kg, and SA 0.9% saline 0.5 mL/kg (n = 9 in each group). Transient forebrain ischemia was induced by hemorrhagic hypotension and carotid artery occlusion, 15 min after administration of lidocaine or saline. The maximal values of glutamate concentration and the areas under glutamate concentration curves in the CA1 were significantly less in the IV lidocaine 10 mg/kg group than the IV saline group, whereas those in the CA1 and the cortex were significantly less in the SA lidocaine 5 and 10 mg/kg groups than the SA saline group. The accumulation of glutamate in the CA1 or the cortex during transient forebrain ischemia was attenuated by IV or SA lidocaine. We conclude that the neuroprotective effect of lidocaine against transient cerebral ischemia involves the suppression of the increase in extracellular glutamate concentration. IV or subarachnoid lidocaine was demonstrated to suppress glutamate accumulation in the hippocampus and the cortex during transient forebrain ischemia in rats by using the dialysis electrode method. Lidocaine can have a neuroprotective effect through the suppression of the increase in extracellular glutamate concentration.