Systemic ketamine blocks cortical spreading depression but does not delay the onset of terminal anoxic depolarization in rats.
Ketamine (KET)-induced blockade of cortical spreading depression (CSD) was examined in rats (n = 51) anesthetized with pentobarbital (50 mg/kg). CSD was elicited by intracortical injection of 1 microliter of 0.15 mol/l potassium acetate 10-40 min after i.p. injection of 6-50 mg/kg KET. KET was almost ineffective at 6 mg/kg but prevented CSD propagation at 12 mg/kg and at higher dosages. The blockade was maximal 20 min after injection. Terminal anoxic depolarization elicited by N2 breathing developed in control rats after a latency which was not significantly different from that in rats pretreated with 50 and 100 mg/kg KET. The failure of CSD blocking dosages of KET to delay the onset of terminal anoxic depolarization indicates that excitotoxic amino acids play different roles in the mechanism of the anoxia-elicited and CSD-related autoregenerative ionic shifts.
Instituto de Investigaciones Fundamentales del Cerebro, Academia de Ciencias de Cuba, Havana.
J
J
Hernándéz-Cáceres
R
R
Macias-González
G
G
Brozek
J
J
Bures
D000818:Animals; D002540:Cerebral Cortex / Q000187:drug effects* / Q000503:physiopathology; D013181:Cortical Spreading Depression / Q000187:drug effects*; D002534:Hypoxia, Brain / Q000503:physiopathology*; D007649:Ketamine / Q000494:pharmacology*; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D051381:Rats
D007649:Ketamine