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

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CAI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)、利多卡闪复合氯胺酮组(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24 h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24 h出现.与Ⅱ组相比,Ⅳ、Ⅴ、Ⅵ组24 h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24 h到48 h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.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

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

Objective To investigate the effect of lidocaine combined ketamine to the cells necrosis and apoptosis in the CA1 region of rat hippoeampus 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), lidoeaine group (Ⅳ, n =16), ke-tamine 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 Wl had significant decreased than group Ⅳ, Ⅴ(P<0.05). The isehemia 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 Ⅵ 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 Li-doeaine combined ketamine can reduce the cell necrosis and apoptosis after global erebral isehemia-reperfusion in rats hippocampus.     

利多卡因对短暂脑缺血后海马区细胞凋亡的影响

目的 探讨利多卡因对短暂脑缺血后海马区迟发性神经元降解的影响。方法 脑缺血模型为兔脑四血管夹闭模型,２５只家兔随机分成三组：假手术组（Ｓｈ,ｎ＝５）;缺血组（Ｉｓ,ｎ＝１０）,夹闭双侧颈总动脉和椎动脉５ｍｉｎ后恢复脑灌注;利多卡因组（Ｌｉ,ｎ＝１０）,夹闭颈总和椎动脉前５ｍｉｎ给予利多卡因１０ｍｇ／ｋｇ。３组均于３ｄ后取脑行病理ＨＥ染色和ＴＵＮＥＬ染色,对民区阳性细胞进行计数。结果 ＨＥ染色发生缺     

外源性一氧化氮对脑缺血-再灌注损伤大鼠海马气体信号分子的影响

目的 研究外源性一氧化氮(NO)对脑缺血-再灌注(I-R)损伤大鼠海马气体信号分子的影响.方法 24只Wistar大鼠随机均分为四组:脑I-R对照组(Ⅰ组),脑I-R+低浓度硝普钠(SNP)组(Ⅱ组)和脑I-R+高浓度SNP组(Ⅲ组),对照组(Ⅳ组).夹闭两侧颈总动脉制作大鼠全脑I-R模型.颈总动脉夹闭前30 min分别腹腔注射SNP 2 mg/kg(Ⅱ组)或4 mg/kg(Ⅲ组).脑缺血20 min,再灌注6 h后处死大鼠,取脑海马组织,检测硫化氢(H_2S)、NO和CO的量和胱硫醚β-合酶(CBS)、血红素氧合酶-1(HO-1)和诱导型一氧化氮合酶(iNOS)活性,以及CKS mRNA、iNOS mRNA和HO-1-mRNA表达水平.结果 Ⅰ、Ⅱ、Ⅲ组大鼠海马中H_2S、NO和CO的含量和CBS、HO和iNOS的活性均高于Ⅳ组;CBS mRNA、iNOS mRNA和HO-1 mRNA表达增高(P<0.05或P<0.01);Ⅱ、Ⅲ组大鼠海马中的上述指标均高于Ⅰ组(P<0.05或P<0.01).结论 外源性NO能诱导脑I-R后大鼠海马CBS mRNA和HO-1 mRNA表达,激活CBS和HO.在脑I-R损伤过程中存在N0对CBS/H2S和HO-1/CO系统的调节.