摘要
目的观察静脉麻醉药依托咪酯对小鼠电惊厥、药物性惊厥的作用,为临床应用提供依据,同时探讨依托咪酯的作用机制。方法以电刺激或致惊剂〔士的宁、N-甲基-D-天冬氨酸(NMDA)、利多卡因〕建立不同类型的小鼠惊厥模型,观察腹腔注射3种剂量的依托咪酯对小鼠强直性惊厥潜伏期、持续期、惊厥发生率、小鼠死亡率以及小鼠存活时间的影响。结果依托咪酯剂量依赖性地缩短电惊厥小鼠强直性惊厥的持续时间,延长士的宁惊厥小鼠的存活时间(P<0.01),较大剂量可完全拮抗NMDA和利多卡因引起的强直性惊厥(P<0.01)。结论依托咪酯对小鼠电惊厥、士的宁、NMDA及利多卡因惊厥均有拮抗作用。依托咪酯的作用机制复杂,可能与NMDA受体、甘氨酸受体、γ-氨基丁酸A(GABAA)受体等有关。
Objeciive To investigate the effect and mectmnism of intravenous anesthetic etomidate on the convulsion induced by electrical stimulation and drugs in mice to provide a theoretical rationale for its clinical application. Methods Three doses of etomidate were administered intraperitoneally. Five minutcs later, convulsion was induced by electricity or drugs [ strychnine/N- methyl- D- aspartate （NMDA）/lidocanine]. The convulsant latency, duration of tonic state, incidence of convulsion, mortality and survival time were noted. Results Etomidate could dose- dependently shorten the duration of tonic state induced by electricity, prolonged the survival time of strychnine - convulsion （ P 〈 0. 01）. The convulsion induced by NMDA and lidocanine could be completely antagonized by big - dose etomidate （ P 〈0. 01）. Conclusions The anticonvulsive effect of etomidate varies in degree in the four experimental models of convulsion. The mechanism of this action may be related to NMDA receptor, glycine receptor and gamma- aminobutyric acid A （GABAA） receptor.
出处
《徐州医学院学报》
CAS
2006年第1期21-23,共3页
Acta Academiae Medicinae Xuzhou
基金
国家自然科学基金资助项目(30471657
39970715)
江苏省自然科学基金资助项目(BK2001143)
