中国实用医药
中國實用醫藥
중국실용의약
CHINA PRACTICAL MEDICAL
2009年
16期
13-15
,共3页
孟晶%段世明%戴体俊%马涛%王丹
孟晶%段世明%戴體俊%馬濤%王丹
맹정%단세명%대체준%마도%왕단
氯胺酮%抗惊厥%定量药物脑电图%δ频段
氯胺酮%抗驚厥%定量藥物腦電圖%δ頻段
록알동%항량궐%정량약물뇌전도%δ빈단
Ketamine%anti-convulsion%Quantitative pharmaco-EEG%δ-band
目的 观察氯胺酮在治疗士的宁诱发惊厥中的作用以及对定量药物脑电图(QPEEG)δ频段的影响.方法 健康家兔50只随机分成生理盐水组(NS组)、氯胺酮1.25 mg/kg(K1.25组)、2.5 mg/kg(K2.5组)、5.0 mg/kg(K5.0组)和苯巴比妥组5.0 mg/kg(PB组),耳缘静脉注射士的宁0.25 mg/kg(15s内注完)制作惊厥模型,一旦强直惊厥出现,立即静脉注射相应的治疗药物.观察各药对家兔的死亡率、强直持续期的影响,并连续监测脑电图,分析QPEEGδ频段功率谱的变化.结果 氯胺酮各剂量组与NS和PB组相比,家兔强直持续期明显缩短(P<0.05, r =0.8696),死亡率为零.脑电图变化与行为学表现同步,NS组在给药后1~5 min几乎所有脑区的δ频段脑电功率百分比较基础值显著降低(P<0.01).PB组在1、2 min时δ功率百分比较基础值降低(P<0.01),5 min时顶枕区开始恢复.氯胺酮各剂量组在给药后多数观察脑区的δ频段功率百分比与基础值相比变化不大,除顶枕区外其他脑区的功率百分比在给药后1~5 min均较NS组和PB组有所提高(P<0.01,P<0.05).结论 氯胺酮抗惊厥的作用主要通过维持额区和颞区脑电δ波频率,减少惊厥时痫性波发放.
目的 觀察氯胺酮在治療士的寧誘髮驚厥中的作用以及對定量藥物腦電圖(QPEEG)δ頻段的影響.方法 健康傢兔50隻隨機分成生理鹽水組(NS組)、氯胺酮1.25 mg/kg(K1.25組)、2.5 mg/kg(K2.5組)、5.0 mg/kg(K5.0組)和苯巴比妥組5.0 mg/kg(PB組),耳緣靜脈註射士的寧0.25 mg/kg(15s內註完)製作驚厥模型,一旦彊直驚厥齣現,立即靜脈註射相應的治療藥物.觀察各藥對傢兔的死亡率、彊直持續期的影響,併連續鑑測腦電圖,分析QPEEGδ頻段功率譜的變化.結果 氯胺酮各劑量組與NS和PB組相比,傢兔彊直持續期明顯縮短(P<0.05, r =0.8696),死亡率為零.腦電圖變化與行為學錶現同步,NS組在給藥後1~5 min幾乎所有腦區的δ頻段腦電功率百分比較基礎值顯著降低(P<0.01).PB組在1、2 min時δ功率百分比較基礎值降低(P<0.01),5 min時頂枕區開始恢複.氯胺酮各劑量組在給藥後多數觀察腦區的δ頻段功率百分比與基礎值相比變化不大,除頂枕區外其他腦區的功率百分比在給藥後1~5 min均較NS組和PB組有所提高(P<0.01,P<0.05).結論 氯胺酮抗驚厥的作用主要通過維持額區和顳區腦電δ波頻率,減少驚厥時癇性波髮放.
목적 관찰록알동재치료사적저유발량궐중적작용이급대정량약물뇌전도(QPEEG)δ빈단적영향.방법 건강가토50지수궤분성생리염수조(NS조)、록알동1.25 mg/kg(K1.25조)、2.5 mg/kg(K2.5조)、5.0 mg/kg(K5.0조)화분파비타조5.0 mg/kg(PB조),이연정맥주사사적저0.25 mg/kg(15s내주완)제작량궐모형,일단강직량궐출현,립즉정맥주사상응적치료약물.관찰각약대가토적사망솔、강직지속기적영향,병련속감측뇌전도,분석QPEEGδ빈단공솔보적변화.결과 록알동각제량조여NS화PB조상비,가토강직지속기명현축단(P<0.05, r =0.8696),사망솔위령.뇌전도변화여행위학표현동보,NS조재급약후1~5 min궤호소유뇌구적δ빈단뇌전공솔백분비교기출치현저강저(P<0.01).PB조재1、2 min시δ공솔백분비교기출치강저(P<0.01),5 min시정침구개시회복.록알동각제량조재급약후다수관찰뇌구적δ빈단공솔백분비여기출치상비변화불대,제정침구외기타뇌구적공솔백분비재급약후1~5 min균교NS조화PB조유소제고(P<0.01,P<0.05).결론 록알동항량궐적작용주요통과유지액구화섭구뇌전δ파빈솔,감소량궐시간성파발방.
Objective To observe the therapeutic action of ketamine and effect on δ-band power of quantitative pharmaco-electroenciphalogram (QPEEG) in strychnine-convulsive rabbits. Methods Convulsion was induced by intravenous strychnine (0.25 mg/kg) within 15 seconds. Rabbits were randomly divided into NS, K1.25, K2.5, K5.0 and PB groups (N=10). Drugs treatment of groups was administered intravenously once convulsion occurred. Mortality and duration of tonic state were noted. The EEG activity was processed with the power spectral analysis. The percentage of power of each frequency band of QPEEG sample was obtained on different time after drug injection. Results Ketamine could dose-dependently short the duration of tonic state induced by strychnine(P<0.05, r =0.8696), and decrease mortality. The percentage of δ-band power in all brain were decreased (P<0.01) in groups of NS within 1~5 minute after therapy. Compare with bases, the percentage of δ-band power decreased within 1~2 minute in PB group, and started to recovery in parietal and occipital region at 5 minute. After ketamine injection, the percentage of δ-band power had no significant change in almost all areas. Compared with NS and PB groups, the percentages of δ-band power in brain areas except parietal and occipital bone were increased within 1~5 minute in three ketamine groups (P<0.05, P<0.01). Conclusion Ketamine has the effect of anti-convulsion and maintain δ band power in forehead and temporal bone to decrease convulsive paroxysm.