缺血预处理对脑缺血再灌注大鼠三叉神经皮层诱发电位的影响
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摘要
比较大鼠三叉神经皮层诱发电位(TEP)和坐骨神经皮层诱发电位(IEP)的特性，观察缺血预处理对脑缺血再灌注大鼠TEP的影响。
电刺激方法检测30只Wistar大鼠TEP和IEP，比较其特性。40只Wistar大鼠，随机分4组，每组10只，采用线栓法闭塞大脑中动脉建立可逆性局灶性脑缺血再灌注模型。假手术组：只做手术操作；单纯预处理组：缺血15min后恢复血流；预处理后缺血组：15min缺血预处理后2天，再次缺血2h再灌注1天；假手术后缺血组：假手术后2天，缺血2h再灌注1天。3天后检测TEP，取脑HE染色。
30只大鼠全部记录到TEP，其中20只记录到IEP。TEP的基本波形为N_1-P-N_2；IEP的基本波形为N-P，N波前可记录到潜伏期小于5ms的P'-N'形干扰波。TEP的N_1、P潜伏期较IEP的N、P潜伏期短，N_1-P波幅较N—P波幅高，有显著性差异，P＜0.001；两者潜伏期的变异系数无明显差异，波幅的变异系数TEP明显小于IEP。N_1、P潜伏期和N_1—P波幅，单纯预处理组与假手术组比较无显著性差异，P＞0.05；预处理后缺血组和假手术后缺血组与假手术组比较潜伏期明显延长，波幅显著下降，有显著性差异，P＜0.01；预处理后缺血组与假手术后缺血组比较潜伏期短，波幅高，有显著性差异，P＜0.05。HE染色假手术组和单纯预处理组未观察到明显的缺血、坏死细胞；预处理后缺血组与假手术后缺血组比较缺血、
延边大学医学院硕士学位论文
中文摘要
坏死细胞明显减少。
TEP较IEP，波形稳定，无干扰波，重复性好，灵敏度高，操作简便。
脑缺血预处理能减轻缺血再灌注后TEP的Nl、P潜伏期延长和N，一P波幅
下降，减轻缺血再灌注损伤;TEP的变化与组织学变化基本一致，是进行
脑缺血预处理的客观监测指标。
Objective: To compare the characteristic of trigeminal evoked potential(TEP) with that of ischiadical evoked potential(IEP) for normal Wistar rat and investigate the influence of cerebral ischemic preconditioning(CIP) on TEP of ischemia-reperfusion rat. Methods: TEPs and lEPs were detected from 30 normal Wistar rats by giving electric stimulation and the characteristic of those compared. Then the animal model of focal cerebral ischemia-reperfusion was established by occluding middle cerebral artery with suture, 40 Wistar rats were randomly divided into four groups: sham-operated group (So, n=10), received operation without cerebral ischemia;,Preconditioning only group(Po> n=10), 15min cerebral ischemia only; Ischemic preconditioning group(Ip> n=10), 15 min cerebral ischemia and 2d reperfusion followed by cerebral ischemia 2h; Cerebral ischemia group(Ci> n=10), operation only and after 2d followed by cerebral ischemia 2h. After Id from last ischemia-reperfusion, TEPs were detected, brain taken out for HE stai
ning. Results: TEP were detected from 30 rats, IEP from 20. The basic waveform of TEP was N1-P-N2 type, IEP was N-P type, but there was P'-N'type interference wave before N. The latencies of N1 , P in TEP were shorter than those of N, P in IEP, the amplitudes of N1-P were bigger than those of N-P, there was significant difference, P < 0.001; there was no significant difference in the coefficient variation of
latencies between TEP and IEP, the amplitudes's coefficient variation of Nj-P were significantly smaller than those of N-P. There were no significant difference in the latencies of N1,. P and the amplitudes of N-P between So and Po, P>0.05; the latencies of N1, P were prolonged, amplitudes of N(-P decreased in Ip and Ci compared with those in So, there were significant difference, P < 0.01; the latencies of N1 , P in Ip were shorter than those in Ci and the amplitude of N1-P in Ip were bigger than those in Ci, there were significant difference, P < 0.05. HE staining showed there were no significant ischemia necrotic neurons in Po and So, the ischemic and infarct volume in Ip were significantly reduced than those in Ci. Conclusion: The waveform of TEP is more stabile, there is no interference wave, its duplication, sensitivity better, the method of its detection more convenient, compared with IEP. CIP could alleviate prolongation of N1, P latency and decrement of Nj-P amplitude, could alleviate the injury of
ischemia-reperfusion; the changes of TEP are basically identical to those of pathology, TEP is objective control standard to CIP.
电刺激方法检测30只Wistar大鼠TEP和IEP，比较其特性。40只Wistar大鼠，随机分4组，每组10只，采用线栓法闭塞大脑中动脉建立可逆性局灶性脑缺血再灌注模型。假手术组：只做手术操作；单纯预处理组：缺血15min后恢复血流；预处理后缺血组：15min缺血预处理后2天，再次缺血2h再灌注1天；假手术后缺血组：假手术后2天，缺血2h再灌注1天。3天后检测TEP，取脑HE染色。
30只大鼠全部记录到TEP，其中20只记录到IEP。TEP的基本波形为N_1-P-N_2；IEP的基本波形为N-P，N波前可记录到潜伏期小于5ms的P'-N'形干扰波。TEP的N_1、P潜伏期较IEP的N、P潜伏期短，N_1-P波幅较N—P波幅高，有显著性差异，P＜0.001；两者潜伏期的变异系数无明显差异，波幅的变异系数TEP明显小于IEP。N_1、P潜伏期和N_1—P波幅，单纯预处理组与假手术组比较无显著性差异，P＞0.05；预处理后缺血组和假手术后缺血组与假手术组比较潜伏期明显延长，波幅显著下降，有显著性差异，P＜0.01；预处理后缺血组与假手术后缺血组比较潜伏期短，波幅高，有显著性差异，P＜0.05。HE染色假手术组和单纯预处理组未观察到明显的缺血、坏死细胞；预处理后缺血组与假手术后缺血组比较缺血、
延边大学医学院硕士学位论文
中文摘要
坏死细胞明显减少。
TEP较IEP，波形稳定，无干扰波，重复性好，灵敏度高，操作简便。
脑缺血预处理能减轻缺血再灌注后TEP的Nl、P潜伏期延长和N，一P波幅
下降，减轻缺血再灌注损伤;TEP的变化与组织学变化基本一致，是进行
脑缺血预处理的客观监测指标。
Objective: To compare the characteristic of trigeminal evoked potential(TEP) with that of ischiadical evoked potential(IEP) for normal Wistar rat and investigate the influence of cerebral ischemic preconditioning(CIP) on TEP of ischemia-reperfusion rat. Methods: TEPs and lEPs were detected from 30 normal Wistar rats by giving electric stimulation and the characteristic of those compared. Then the animal model of focal cerebral ischemia-reperfusion was established by occluding middle cerebral artery with suture, 40 Wistar rats were randomly divided into four groups: sham-operated group (So, n=10), received operation without cerebral ischemia;,Preconditioning only group(Po> n=10), 15min cerebral ischemia only; Ischemic preconditioning group(Ip> n=10), 15 min cerebral ischemia and 2d reperfusion followed by cerebral ischemia 2h; Cerebral ischemia group(Ci> n=10), operation only and after 2d followed by cerebral ischemia 2h. After Id from last ischemia-reperfusion, TEPs were detected, brain taken out for HE stai
ning. Results: TEP were detected from 30 rats, IEP from 20. The basic waveform of TEP was N1-P-N2 type, IEP was N-P type, but there was P'-N'type interference wave before N. The latencies of N1 , P in TEP were shorter than those of N, P in IEP, the amplitudes of N1-P were bigger than those of N-P, there was significant difference, P < 0.001; there was no significant difference in the coefficient variation of
latencies between TEP and IEP, the amplitudes's coefficient variation of Nj-P were significantly smaller than those of N-P. There were no significant difference in the latencies of N1,. P and the amplitudes of N-P between So and Po, P>0.05; the latencies of N1, P were prolonged, amplitudes of N(-P decreased in Ip and Ci compared with those in So, there were significant difference, P < 0.01; the latencies of N1 , P in Ip were shorter than those in Ci and the amplitude of N1-P in Ip were bigger than those in Ci, there were significant difference, P < 0.05. HE staining showed there were no significant ischemia necrotic neurons in Po and So, the ischemic and infarct volume in Ip were significantly reduced than those in Ci. Conclusion: The waveform of TEP is more stabile, there is no interference wave, its duplication, sensitivity better, the method of its detection more convenient, compared with IEP. CIP could alleviate prolongation of N1, P latency and decrement of Nj-P amplitude, could alleviate the injury of
ischemia-reperfusion; the changes of TEP are basically identical to those of pathology, TEP is objective control standard to CIP.
引文
1. Kitagawa K, Matsumoto M, Tagaya M, et al. Ischemic tolerance phenomenon found in the brain. Brain Res, 1990, 528(1): 21-26
2. Moncayo J, de Freitas GR, Bogousslavsky, et al. Do transient ischemic attacks have a neuroprotective effect? Neurology, 2000, 54(11): 2089-2094
3．臧人和，梁维帮，朱苏然．实验性脑缺血时体感诱发电位和细胞超微结构的变化．中华神经外科杂志，1995，11(2)：91-96
4. Astrup J. Energy-requiring cell functions in the ischemic brain. J Neurosurg, 1981,72:1482-1487
5. Meyer KL, Demprey RL, Rog MW. Somatosensory evoked potentials as measure of experimental cerebral ischemia. J Neurosurg, 1985, 62: 269-273
6．金魁赫．大鼠三叉神经诱发电位的特征及通路的分析．医学博士论文．1999：25-26
7．张杰文，索爱琴．皮质诱发电位正常参考值实验研究．河南实验神经疾病杂志，2000，3(6)：8-9
8．焦桌敏，赵瑞波，毕彦忠，等．大鼠脑局灶性预缺血对再次缺血的影响．中风与神经疾病杂志，1999，16(3)：210-215
9. Longar EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral atery occlusion without craniectomy in rats[J]. Stroke, 1989, 20(1): 1-8
10．王瑞．大鼠脑皮质诱发电位记录法．山西医学院学报，199l，2：148-14
11．苅田典生．觉醒时体性感觉诱発电位记录．脑波筋电图，1989，17(3)：248-252
12. Sakatani K, Lizuka H, Yong W. Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occusion. Stroke, 1990, 21: 124-132
13. Prior PE. EEG monitoring and evoked potentials in brain ischemia. Brain J Anaesh, 1985, 57(1): 63-69
14. Masada T, Hua Y, Xi G, et al. Attention of ischemic brain edema and cerebrovascular injury after ischemic preconditioning in the rat. J Cereb Blood Flow Metab, 2001, 21(1): 22-33
15. Faught E. Current role of of electroencephalography in cerebral ischemia. Stroke, 1993, 24: 609-614
16. Heiss WD. Experimental evidence of ischemic threeesholds and functional recovery. Stroke, 1992, 23: 1668-1674
17. Heurterux C, Lauritzen I, Widmann C, et al. Essential role of adenosine, ade-nosine A1 receptors, and ATP-sensitive K~+ channels in cerebral ischemic preconditioning. Proc Natl Acad Sci Usa, 1995, 92(10): 4666-4670
18. Jay G. Shake MD, Eric A. Peck MD, Eduardo Marban MD, et al. Pharmacologically induced preconditioning with diazoxide: a novel approach to brain protection. Ann Thorac surg, 2001, 72:1849-1854
19．王晓斌．预缺血处理对脑保护的实验研究进展．医学综述，2000，6(8)：
358-359
20. Hakin AM. Could transient ischemic attacks have cerebro- protection role? Stroke, 1994, 25: 715-716
21. Shimizu S, Nagayama T, jin KL, et al. Bcl-2 antisense treatment prevents induction of tolerance to focal ischemia in rat. J Cereb Blood Flow Metab, 2001, 21(3): 233-243
22．王锷，郭曲练，谭秀娟，等．Bcl-2和Bax蛋白在大鼠脑缺血预处理脑组织中的表达．湖南医科大学学报，2001，26(3)：217-218
23. Chen J, Simon R. Ischemic to tolerlance in the brain. Neurology, 1997, 48(3): 306-311
24. Currie RW, Ellison JA, White RF. Benign focal ischemic preconditioning induces neuronal hsp70 and prolonged astrodisis with expression ofhsp70. Brain Res, 2000, 863(1-2): 169-181
25. Centeno JM, Salom JB. Nitric oxide is involved in anoxic preconditioning neuroprotection in rat hippocampal slices. Brain Res, 1999, 836(1-2): 62-69
26．陈连壁，崔敏，夏作理，等．脑缺血预适应过程中大鼠脑血液NO含量的动态变化．中国微循环，1999，3(4)：255-261
27．赵纲，邓艳秋，焦桌敏，等．局灶性脑缺血预处理对再次缺血后微血管损伤及脑水肿的保护作用．哈尔滨医科大学学报，2002，36(3)：209-211
2. Moncayo J, de Freitas GR, Bogousslavsky, et al. Do transient ischemic attacks have a neuroprotective effect? Neurology, 2000, 54(11): 2089-2094
3．臧人和，梁维帮，朱苏然．实验性脑缺血时体感诱发电位和细胞超微结构的变化．中华神经外科杂志，1995，11(2)：91-96
4. Astrup J. Energy-requiring cell functions in the ischemic brain. J Neurosurg, 1981,72:1482-1487
5. Meyer KL, Demprey RL, Rog MW. Somatosensory evoked potentials as measure of experimental cerebral ischemia. J Neurosurg, 1985, 62: 269-273
6．金魁赫．大鼠三叉神经诱发电位的特征及通路的分析．医学博士论文．1999：25-26
7．张杰文，索爱琴．皮质诱发电位正常参考值实验研究．河南实验神经疾病杂志，2000，3(6)：8-9
8．焦桌敏，赵瑞波，毕彦忠，等．大鼠脑局灶性预缺血对再次缺血的影响．中风与神经疾病杂志，1999，16(3)：210-215
9. Longar EZ, Weinstein PR, Carlson S, et al. Reversible middle cerebral atery occlusion without craniectomy in rats[J]. Stroke, 1989, 20(1): 1-8
10．王瑞．大鼠脑皮质诱发电位记录法．山西医学院学报，199l，2：148-14
11．苅田典生．觉醒时体性感觉诱発电位记录．脑波筋电图，1989，17(3)：248-252
12. Sakatani K, Lizuka H, Yong W. Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occusion. Stroke, 1990, 21: 124-132
13. Prior PE. EEG monitoring and evoked potentials in brain ischemia. Brain J Anaesh, 1985, 57(1): 63-69
14. Masada T, Hua Y, Xi G, et al. Attention of ischemic brain edema and cerebrovascular injury after ischemic preconditioning in the rat. J Cereb Blood Flow Metab, 2001, 21(1): 22-33
15. Faught E. Current role of of electroencephalography in cerebral ischemia. Stroke, 1993, 24: 609-614
16. Heiss WD. Experimental evidence of ischemic threeesholds and functional recovery. Stroke, 1992, 23: 1668-1674
17. Heurterux C, Lauritzen I, Widmann C, et al. Essential role of adenosine, ade-nosine A1 receptors, and ATP-sensitive K~+ channels in cerebral ischemic preconditioning. Proc Natl Acad Sci Usa, 1995, 92(10): 4666-4670
18. Jay G. Shake MD, Eric A. Peck MD, Eduardo Marban MD, et al. Pharmacologically induced preconditioning with diazoxide: a novel approach to brain protection. Ann Thorac surg, 2001, 72:1849-1854
19．王晓斌．预缺血处理对脑保护的实验研究进展．医学综述，2000，6(8)：
358-359
20. Hakin AM. Could transient ischemic attacks have cerebro- protection role? Stroke, 1994, 25: 715-716
21. Shimizu S, Nagayama T, jin KL, et al. Bcl-2 antisense treatment prevents induction of tolerance to focal ischemia in rat. J Cereb Blood Flow Metab, 2001, 21(3): 233-243
22．王锷，郭曲练，谭秀娟，等．Bcl-2和Bax蛋白在大鼠脑缺血预处理脑组织中的表达．湖南医科大学学报，2001，26(3)：217-218
23. Chen J, Simon R. Ischemic to tolerlance in the brain. Neurology, 1997, 48(3): 306-311
24. Currie RW, Ellison JA, White RF. Benign focal ischemic preconditioning induces neuronal hsp70 and prolonged astrodisis with expression ofhsp70. Brain Res, 2000, 863(1-2): 169-181
25. Centeno JM, Salom JB. Nitric oxide is involved in anoxic preconditioning neuroprotection in rat hippocampal slices. Brain Res, 1999, 836(1-2): 62-69
26．陈连壁，崔敏，夏作理，等．脑缺血预适应过程中大鼠脑血液NO含量的动态变化．中国微循环，1999，3(4)：255-261
27．赵纲，邓艳秋，焦桌敏，等．局灶性脑缺血预处理对再次缺血后微血管损伤及脑水肿的保护作用．哈尔滨医科大学学报，2002，36(3)：209-211