This experiment evaluated the potential for ketamine HCl, a non-competitive glutamate antagonist, to minimize injury resulting from temporary focal cerebral ischemia. Male spontaneously hypertensive rats were randomly assigned to receive either ketamine (n = 13) or halo hane anesthesia (n = 12) during 2 h reversible middle cerebral artery occlusion (MCAO). Ketamine was administered as a 50 mg/kg i.v. loading dose followed by a continous 1.25 mg/kg/min i.v. infusion beginning 25 min prior to ischemia and continued until 30 min after reperfusion. An additional group of rats (ketamine-shmas, n = 8) underwent craniectomy and ketamine administration (as above) but the middle cerebral artery was not ligated. Physiologic values were similar between groups with the exception of plasma glucose which was elevated in the halothane-MCAO group. After 4 days recovery. rats in all groups were neurologically evaluated. There were no differences between the two groups undergoing MCAO for neurologic grading or open field behavior, although both groups performed worse than did ketamine-shams (P < 0.05). In contrast, motor performance revealed more severe deficits in the ketamine-MCAO rats vs either the halothane-MCAO or ketamine-sham groups (P < 0.05). Cerebral infare volume was then planimetrically measured after triphenyl tetrazolium chloride (TTC) stining of fresh brain sections. Mean ± S.D. infarct volume was not different between the halothane-MCAO (134 ± 51 mm3) and ketamine-MCAO (131 ± 64 mm3) groups. Seven of 8 sham rats were free of TTC demarcated injury and in the remaining rat injury was minimal. These results indicate that under conditions of reversible focal ischemia, pretreatment with ketamine HCl offers no protective benefit over halothane anesthesia.
- Anesthetic, intravenous
- Brain ischemia