Myslobodsky M S, Golovchinsky V, Mintz M
Pharmacol Biochem Behav. 1981 Jan;14(1):27-33. doi: 10.1016/0091-3057(81)90099-x.
Ketamine hydrochloride in doses producing narcotic-cataleptic effects (50--100 mg/kg, IP) reduced the intensity of picrotoxin convulsions and eliminated seizures caused by metrazol administration. Subcataleptic doses (5--20 mg/kg) increased the duration of mitigated convulsive symptoms (abortive grand mal fits, jerks) especially those evoked by picrotoxin. Narcotic-cateleptic doses of ketamine considerably increased the duration of the period of single and multiple jerks produced by picrotoxin administration. Both convulsants transformed 1--2 Hz "ketamine complexes" into 2--4 Hz Wave spike discharges which appeared in a quasi-periodic fashion alternating with periods of relatively suppressed electrocortical activity. Electroencephalographic grand mal patterns were typically dissociated from behavioral manifestations under 50--100 mg/kg of ketamine, followed by a short period of postictal depression and a rapid recovery of preseizure electrographic patterns. Findings suggest that mechanisms involved in seizure alleviation may be responsible for sustaining mitigated convulsive phenomena. Neuro-chemical processes underlying antiepileptic ketamine potency remain unknown.
盐酸氯胺酮以产生麻醉性木僵效应的剂量(50 - 100毫克/千克,腹腔注射)可降低苦味毒惊厥的强度,并消除由戊四氮给药引起的癫痫发作。亚麻醉剂量(5 - 20毫克/千克)可延长减轻的惊厥症状(顿挫性癫痫大发作、抽搐)的持续时间,尤其是由苦味毒诱发的症状。麻醉性木僵剂量的氯胺酮可显著延长由苦味毒给药产生的单次和多次抽搐的持续时间。两种惊厥剂都将1 - 2赫兹的“氯胺酮复合波”转变为2 - 4赫兹的棘波放电,这种放电以准周期性方式出现,与相对抑制的皮质电活动期交替。在50 - 100毫克/千克氯胺酮作用下,脑电图癫痫大发作模式通常与行为表现分离,随后是短暂的发作后抑郁期,并迅速恢复到发作前的脑电图模式。研究结果表明,参与缓解癫痫发作的机制可能是维持减轻的惊厥现象的原因。氯胺酮抗癫痫效力的神经化学过程尚不清楚。