期刊文献+

氯胺酮治疗难治性癫痫持续状态的研究进展 被引量:2

Research progress of ketamine in refractory status epileptieus
原文传递
导出
摘要 背景难治性癫痫持续状态(refractory status epileptieus,RSE)发病机制不明,具有高致残率和致死率。大量研究发现氯胺酮对RSE具有良好的治疗效果。目的综述RSE发病机制、氯胺酮用于治疗RSE的研究进展以及其副作用的防止策略,为氯胺酮的临床应用提供参考。内容RSE的发病机制主要与γ-氧基丁酸(γ-aminobutyric acid,GABA)受体的变化、谷氨酸(glutamine,Glu)过量释放等有关。氯胺酮复合用药能够安全有效地终止RSE发作。趋向氯胺酮复合用药早期介入RSE的治疗可能改善其结局,其远期应用前景尚需进一步研究。 Backgroud Because the underlying molecular mechanism remains poorly understood, there is no effective treatment for refractory status epileptieus (RSE). Thus overall mortality for RSE has been reported up to 50%. However, several studies have demonstrated that ketamine could be an effective drug for stopping RSE. Objective To summarize the underlying molecular mechanism of RSE and explore researches of ketamine used in RSE, aiming at providing practical advice for clinical application. Content The molecular mechanism of RSE was attributed to abnormal γ-aminobutyric acid (GABA) receptor or excessive releasing of Glu and so on. Ketamine combined with other antiepileptic drugs could stop RSE safely and effectively. Trend Early application of ketamine combined with other antiepileptic drugs could prove prognosis of RSE and its application prospect should be further studied.
出处 《国际麻醉学与复苏杂志》 CAS 2016年第4期344-348,共5页 International Journal of Anesthesiology and Resuscitation
基金 重庆市应用开发项目(cstc2014yykfA110028) 卫生部国家临床重点专科建设项目[财社(2011)170] 重庆市医学重点学科项目[渝卫科教(2007)2]
关键词 难治性癫痫持续状态 氯胺酮 γ氧基丁酸 N-甲基-D-天冬氨酸 Refractory status epileptieus Ketamine γ-aminobutyric acid N-Methyl-D-Aspartate
  • 相关文献

参考文献36

  • 1Vignatelli L, Tonon C, D'Alessandro R, et al. Incidence and short-term prognosis of status epileptieus in adults in Bologna, Italy [J]. Epilepsia, 2003, 44 (7): 964-968. DOI:10.1046/j.1528- 1157.2003.63702.x.
  • 2Lowenstein DH, Bleck T, Macdonald RL. It's time to revise the definition of status epilepticus [J]. Epilepsia, 1999, 40 (1): 120- 122. DOI:10.1111/j.1528-1157.1999.tb02000.x.
  • 3Dorandeu F, Dhote F, Barbier L, et al. Treatment of status epilepticus with ketamine, are we there yet? [J]. CNS Neurosci Ther, 2013, 19(6): 411-427. DOI:10.1111/cns.12096.
  • 4Naylor DE, Liu H, Wasterlain CG. Trafficking of GABAA receptors, loss of inhibition, and a mechanism for pharmacoresistance in status epilepticus[J]. J Neurosci, 2005, 25 (34): 7724-7733. DOI:10.1523/JNEUROSCI.4944-04.2005.
  • 5Meierkord H, Boon P, Engelsen B, et al. EFNS guideline on the management of status epilepticus in adults[J]. Eur J Neurol, 2010, 17(3): 348-355. DOI:10.1111/j.1468-1331.2009.02917.x.
  • 6Fujikawa DG. Prolonged seizures and cellular injury: understanding the connection[J]. Epilepsy Behav, 2005, 7(3): 3-11. DOI:http:// dx.doi.org/10.1016/j .yebeh.2005,08.003.
  • 7Murthy JM. Refractory status epilepticus [J]. Neurol India, 2006, 54(4): 354-358. DOI:10.4103/0028-3886.28104.
  • 8Wasterlain CG, Liu H, Naylor DE, et al. Molecular basis of self- sustaining seizures and pharmacoresistance during status epilepticus: the receptor trafficking hypothesis revisited [J]. Epilepsia, 2009, 50 (Suppl 12): 16-18. DOI: 10.1111/j. 1528-1167. 2009.02375.x.
  • 9Rice AC, DeLorenzo RJ. NMDA receptor activation during status epilepticus is required for the development of epilepsy [J]. Brain Res, 1998, 782 (1-2): 240-247. DOI:10.1016/S0006 -8993 (97) 01285-7.
  • 10Rizzi M, Caccia S, Guiso G, et al. Limbic seizures induce P-glycoprotein in rodent brain: functional implications for pharmacoresistance[J]. J Neurosci, 2002, 22(14): 5833-5839.

二级参考文献30

  • 1王士凡 孙定人 王功立 等编译.药物不良反应.第一版[M].北京:人民卫生出版社,1992.430-431.
  • 2Eide PK, Stubhaug A. Relief of glossopharyngeal neuralgia by ketamine- induced N -methyl -aspartate receptor blockade. Neumsurgery, 1997, 41 (2): 505-508.
  • 3Chizh BA. l~w dose ketamine: a therapeutic and research tool to explore N-methyl-D-aspartate (NMDA) receptor-mediated plasticity in pain pathways. J Psychopharmacal, 2007, 21(3): 259-271.
  • 4Sigtermans M J, van Hilten JJ, Bauer MC, et al. Ketamine produces effective and long-term pain relief in patients with complex regional pain syndrome Type 1. Pain, 2009, 145(3): 304-311.
  • 5Bell RE Ketamine for chronic non-cancer pain. Pain, 2009, 141(3): 210-214.
  • 6Bergman SA. Ketamine: review of its pharmacology and its use in pediatric anesthesia. Anesth Prog, 1999, 46(1 ): 10-20.
  • 7Gonzales JM, Loeb AL, Reichard PS, et al. Ketamine inhibits glutamate-, N --methyl -D --aspartate -, and quisqualate -stimulated cGMP production in cultured cerebral neurons. Anesthesiology, 1995, 82( 1 ) : 205-213.
  • 8Kawasaki T, Ogata M, Kawasaki C, et al. Ketamine suppresses proinflammatory cytokine production in human whole blood in vitro. Anesth Analg, 1999, 89(3): 665-669.
  • 9Shapira Y, Artru AA, Lain AM. Ketamine decreases cerebral infarct volume and improves neurological outcome following experimental head trauma in rats. J Neurosurg Anesthesiol, 1992, 4 (4): 231- 240.
  • 10Miyamoto E, Nakao S, Tomimoto H, et al. Ketamine attenuates hypocapnia-induced neuronal damage in the caudoputamen in a rat model of chronic cerebral hypoperfusion. Neurosci Lett, 2004, 354 (1): 26-29.

共引文献71

同被引文献27

引证文献2

二级引证文献1

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部