期刊文献+

利多卡因复合氯胺酮对全脑缺血大鼠海马细胞凋亡的影响 被引量:2

Effects of lidocaine combined ketamine on apoptosis in hippocampus following global cerebral ischemic-reperfusion injury in rats
原文传递
导出
摘要 目的研究利多卡因复合氯胺酮对全脑缺血,再灌注大鼠海马CA1区细胞坏死和凋亡的影响。方法Wistar大鼠60只,随机分为6组:对照组(Ⅰ组,n=4)、假手术组(Ⅱ组,n=4)、模型组(Ⅲ组,n=4)、利多卡因组(Ⅳ组,n=16)、氯胺酮组(Ⅴ组,n=16)、利多卡因复合氯胺酮组(Ⅵ组,n=16),采用四血管阻断法制备全脑缺血,再灌注模型。Ⅳ、Ⅴ、Ⅵ组在夹闭血管前15min分别腹腔注射利多卡因10mg/kg、氯胺酮10mg/kg或利多卡因复合氯胺酮混合液10mg/kg。再灌注12、24、48、72h后行HE染色和细胞凋亡(TUNEL法)检测,观察大鼠海马CA1区细胞坏死和凋亡。结果与Ⅱ组比较,Ⅳ、Ⅴ、Ⅵ组24h缺血神经元显著增多,差异有统计学意义(P〈0.05);Ⅵ组缺血神经元较Ⅳ、Ⅴ组显著减少,差异有统计学意义(P〈0.05),Ⅳ、Ⅴ组间无统计学差异,缺血神经元高峰在24h出现。与Ⅱ组相比,Ⅳ、Ⅴ、Ⅵ组24h凋亡细胞显著增多,差异有统计学意义(P〈0.05),Ⅵ组细胞凋亡数较Ⅳ、Ⅴ组减少,差异有统计学意义(P〈0.05);Ⅳ、Ⅴ组间无统计学差异,细胞凋亡高峰在24h到48h间,此后,随再灌注时间的延长而减少。结论利多卡因复合氯胺酮可减少和降低脑缺血/再灌注后大鼠神经细胞坏死和凋亡的发生。 Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippocampus following global cerebral ischemia-reperfusion. Methods Sixty adult Wistar rats were randomly divided into 6 groups:control group(Ⅰ, n=4),sham operation group (Ⅱ, n=4), model group (Ⅲ, n =4), lidocaine group (Ⅳ, n =16), ketamine group(Ⅴ, n=16), lidocaine and ketamine group (Ⅵ, n=16). The global cerebral ischemia ( 10 min) was induced by the use of the four-vessel occlusion method. Group Ⅳ,Ⅴ,Ⅵ intraperitoneally injected the lidocaine 10mg/kg, ketamine 10 mg/kg or lidocaine combined ketamine 10 mg/kg. The effect of cells necrosis and apoptosis was detected by using HE staining and TUNEL methods. Results Compared with group Ⅱ the numbers of ischemia neuron of group Ⅳ, Ⅴ, Ⅵ had significant deviation (P〈0.05) in 24 h, and group Ⅵ had significant decreased than group Ⅳ,Ⅴ(P〈0.05). The ischemia neurons peak presented in 24 h. Compared with group Ⅱ the numbers of apoptosis of group Ⅳ, Ⅴ, Ⅵ had significantly deviation (P〈0.05)in 24 h, and group Ⅶ had significantly decreased than group Ⅳ,Ⅴ (P〈0.05). The apoptosis peak presented in 24 h and 48 h, and decreased during reperfusion time. Conclusion Lidocaine combined ketamine can reduce the cell necrosis and apoptosis after global crebral ischemia-reperfusion in rats hippocampus.
出处 《国际麻醉学与复苏杂志》 CAS 2009年第3期206-209,共4页 International Journal of Anesthesiology and Resuscitation
关键词 利多卡因 氯胺酮 脑缺血 再灌注 海马 细胞凋亡 Lidocaine Ketamine Ischemic-reperfusion Hippocampus Apoptosis
  • 相关文献

参考文献9

二级参考文献64

共引文献38

同被引文献27

  • 1吴忧,贾建平.脑缺血动物模型的制备及影响因素[J].中国脑血管病杂志,2007,4(1):42-46. 被引量:12
  • 2庄心良,曾因明,陈伯銮,等.现代麻醉学[M].3版.北京:人民卫生出版社,2009:925.
  • 3James G. Anesthetic pharmacology:reflections of a section editor [ J ]. Anesth Analg,2007,105 (5) : 1186 - 1190.
  • 4Himmelseher S, Durieux ME. Revising a dogma: ketamine for patients with neurological injury? [ J ]. Anesth Analg, 2005, 101 (3) :524 -534.
  • 5Proescholdt M, Heimann A, Kempski O. Neuron protection of S ( + ) ketamine isomer in global forebrain ischemia[ J ]. Brain Res,2001,904 ( 3 ) :245 - 251.
  • 6Joshi S, Wang M, Nishanian EV. et al. Electrocerebral silence byintraearotid anesthetics does not affect early hyperemia after transient cerebral ischemia in rabbits [ J ]. Anesth Analg, 2004, 98(5) :1454 - 1459.
  • 7Monassier L, Tibirica E, Roegel JC, et al. Prevention by NMDA receptor antagonists of the centrally-evoked increases of cardiac inotropic responses in rabbits [ J ]. Br J Pharmacol, 1994, 111 (4) :1347 - 1354.
  • 8Han J, Kim N, Joo H, et al. Ketamine abolishes ischemic preconditioning through inhibition of K(ATP) channels in rabbit hearts [ J ]. AM J Physiol Heart Circ Physiol, 2002,283 ( 1 ) : H13 -H21.
  • 9Pietrzak B, Czarnecka E. Effect of combined administration of ethanol and tiagabine on rabbit EEG [ J]. Pharmacol Rep, 2006, 58(6) :890 -899.
  • 10Wang M, Agarwal S, Mayevsky A, et al. Optically measured NADH concentrations are unaffected by propofol induced EEG silence during transient cerebral hypoperfusion in anesthetized rabbits [ J ]. Brain Res ,2011,1396:69 - 76.

引证文献2

二级引证文献21

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