翼点入路在构建视神经损伤动物模型中的应用

目的探讨翼点入路在构建视神经损伤动物模型实验中的可行性。方法成年健康猫36只,按损伤时间分为正常、6h、1d、3d、7d、14d6个组,每组6只。模仿临床上翼点入路显微手术,暴露视神经,以无创血管夹夹持20s,于此后不同时间取视神经标本,应用免疫组化染色检测视神经胶质纤维酸性蛋白(GFAP)、神经丝蛋白(NF)及髓鞘碱性蛋白(MBP)表达,观察视神经损伤后的病理改变。结果视神经损伤后损伤侧瞳孔较正常瞳孔变大,直接对光反射消失,间接对光反射存在,直接钳夹损伤区GFAP、NF和MBP染色均减弱。结论采用翼点入路构建视神经损伤动物模型有临床及理论依据。视神经损伤后直接损伤区星形胶质细胞死亡,NF减少,髓鞘脱失。     

猫慢性视神经压迫损伤模型的建立

目的建立猫慢性视神经压迫损伤动物模型。方法成年健康猫20只,按置入球囊内注入不同剂量造影剂分为健康对照组、0.2ml、0.25ml、0.35ml 4个组,每组5只。模仿临床上翼点入路,显微手术暴露视神经后,置入充盈的不可脱球囊于其下,后接导管,以注入造影剂的方式控制球囊大小,形成类似鞍区肿瘤占位,并辅以CT和视觉诱发电位检查,研究慢性视神经损伤前后视觉电生理方面的变化。以上动物按分组处死后,取视神经标本,进行电镜分析,研究视神经损伤后的病理改变。结果早期(术后2周),因占位病变(0.2cm3)在颅内代偿范围内,视觉诱发电位改变不明显。术后4周颅内占位达0.3cm3时超出颅内代偿空间,视觉诱发电位改变,颅内占位达0.35cm3时视觉诱发电位改变更为明显,表现为P1波潜伏期明显延长,振幅明显减小。结论首次建立的慢性颅内段视神经压迫损伤模型稳定,可模仿鞍区肿瘤引起的视神经病变,慢性视神经压迫的视觉诱发电位改变呈渐进性,早期在代偿范围内改变并不明显,晚期表现为P1波潜伏期延长,振幅减小,如不去除压迫难以恢复。     

神经干细胞移植对大鼠损伤视神经超微结构的实验研究

目的 探讨神经干细胞(NSCs)移植治疗视神经损伤的新方法,为治疗视神经损伤打下基础.方法 制作视神经损伤大鼠模型,分别在急性损伤期和损伤后4周一次性向视神经受损区鞘膜内注射NSCs.注射后4周断颈处死动物,在电镜下观察损伤视神经超微结构.结果 损伤后视神经轴突减少,伴有水泡样变性,髓鞘厚薄不一,结构疏松,局部有缺损破碎,出现脱髓鞘现象,基质增多.NSCs移植组轴突数目增多,水泡样变性少见,髓鞘修复基本完整;延期移植组更加明显:对照组轴突变得透明空虚,髓鞘变成薄膜样结构,可见到鞘膜泡状分离和碎屑,基质成分明显增多.结论 NSCs移植可使损伤视神经超微结构得到有效修复,其有望成为治疗视神经损伤的有效手段.     

改良翼点入路手术减压治疗视神经损伤

目的 探讨颅脑损伤合并视神经损伤手术入路及减压的范围。方法 改良翼点入路开颅手术治疗22例颅损伤合并视神经损伤患者，术中磨除骨性视神经管周径1／2，切开视神经鞘膜、总腱环及镰状韧带，视神经充分减压。视力恢复评价标准：黑矇、光感、眼前手动、眼前数指和能见标字视力表符号5个级别，术后视力提高2个级别以上者为有效。结果 术后3～6月随访，有效率为81．8％。结论 改良翼点入路手术减压治疗视神经损伤效果良好，术后视力恢复与伤后手术时间、手术方法及减压范围有关，亦与其原发损伤程度密切相关。     

管内段视神经损伤后视网膜的形态学改变及GAP-43的表达

背景：视神经损伤后,视网膜发生一系列复杂的病理变化,从而造成功能丧失。 目的：观察管内段视神经损伤后视网膜的病理变化,比较视神经管减压术和激素对管内段视神经损伤的治疗作用。 设计、时间及地点：不同实验因素作用下视网膜病理形态学对比观察。实验于2008-09/11在潍坊医学院解剖学教研室完成。 材料：健康成年家兔36只,应用金属圆柱体自由落体冲击法建立兔右眼管内段视神经损伤模型。 方法：随机抽签法将实验兔分为单纯损伤组（n=24）,治疗组（n=12）。利用免疫组织化学、图像分析等技术,观察神经损伤后1、3、5、7、14 d及视神经管减压术、地塞米松、视神经管减压术＋地塞米松治疗14 d后,视网膜的形态学改变及GAP-43的表达。 主要观察指标：视神经损伤后RGCs记数及视网膜GAP-43表达阳性细胞记数的变化。 结果：纳入实验兔36只均进入结果分析。视神经损伤1 d后,RGCs平均记数轻度下降;损伤3、5、7 d时,RGCs数分别为对照组的84.48% 、72.23% 、57.46%;14 d时,节细胞仅有15.43％存活。损伤后3 d,视网膜切片中可见GAP-43表达阳性的细胞;伤后5 d阳性细胞增多;伤后7 d阳性细胞数和积分光密度值达最高峰;伤后14 d阳性细胞数下降。经手术减压、激素治疗、激素＋手术治疗后,RGCs存活率分别为36.01%、32.78%、56.98%。 结论：管内段视神经损伤后RGCs出现渐进性退变,数量逐渐减少;视神经管减压术和激素对管内段视神经损伤有一定的治疗作用,其疗效明显优于只采用一种方法。     

兔视神经损伤后谷氨酸对视网膜的兴奋毒性损伤作用研究

目的探讨家兔视神经损伤后谷氨酸浓度变化对视网膜的兴奋毒性及其作用机制。方法 40只健康雄性日本大耳白家兔随机分成2组,A组35只,B组5只。A组家兔左眼为实验制备视神经损伤模型,右眼为对照眼。B组家兔双眼同时制备视神经损伤模型。分别于第1、3、7、14及28d随机处死A组7只家兔及B组1只家兔,检测家兔实验眼和对照眼视网膜谷氨酸浓度,并观察B组家兔视网膜病理形态学改变。结果家兔视神经损伤后视网膜内谷氨酸浓度逐渐升高,3d达到高峰,14d时家兔实验眼视网膜谷氨酸浓度仍高于对照眼(p<0.05),28d时其视网膜谷氨酸浓度无统计学差异(p>0.05)。家兔视网膜病理形态学观察:视神经损伤后1d,神经节细胞排列紊乱;3～7d,视网膜节细胞大量空泡化;7d～14d,视网膜厚度变薄,神经节细胞减少;14d后视网膜各层细胞改变逐步趋于稳定。结论家兔视神经损伤后,视网膜谷氨酸浓度升高是视网膜神经节细胞继发损伤的原因之一。     

视神经损伤动物模型的研制方法

视神经损伤是头部损伤的严重伴随损伤 ,对于视神经损伤的诊断和治疗 ,目前尚无成熟、统一认识。国内外学者的研究也多侧重于临床 ,基础工作所做甚少。而视神经损伤动物模型的研制 ,则是进行有关视神经损伤基础研究工作首先所面临的一个重要课题。国内外学者经过大量的探索 ,研制出了一系列各具特色的视神经损伤动物模型 ,现将其综述如下。1　各种类型的视神经损伤动物模型1 1　视神经横断伤动物模型　视神经横断伤动物模型〔1 -3〕是各种视神经损伤动物模型中最易建立 ,亦是最易于统一损伤标准的动物模型。该动物模型建立方法一般多为 :动物…     

复发缓解型EAE大鼠长期、自然病程的视神经病理改变

目的建立小剂量复合抗原成分诱导的EAE长病程动物模型,通过多种方法观察EAE大鼠的视神经病理改变。方法雌性Wistar大鼠72只,6~8周龄,体重180~200g,其中12只为对照组,余60只诱导EAE模型,进行EAE动物的神经功能评分(按照Kono五级评分法[1]进行),观察大鼠每次发病时的病情、病程变化。于第一次发病后第7d和半年时行眼底照相检查,并取视神经行HE染色光镜观察和透射电镜观察其病理改变。结果 EAE组大鼠视神经光镜主要表现为有不同程度的炎症反应;电镜主要表现为髓鞘稀疏,其髓鞘板层松解,轴突萎缩、变性,结构模糊不清。EAE组第一次发病后第7d及半年时眼底照相提示视乳头萎缩,边界不清楚。半年时视乳头萎缩更明显。结论 EAE大鼠存在明显的视神经病变,主要表现为视神经炎症反应、脱髓鞘改变和轴索损伤。     

经颅视神经管减压术治疗视神经损伤

目的探讨经翼点入路行视神经管减压术治疗外伤性视神经损伤的方法及临床疗效。方法对年月至年4月我们收治的6例外伤性视神经损伤患者经翼点入路行视神经管减压治疗。结果 4例术前视力呈眼前指动及以上者,术后分别随访3～23个月,均提升至0.4以上;2例术前失明患者,术后随访半年视力无改善。结论经翼点入路行视神经管减压术治疗外伤性视神经损伤可获得较好疗效。     

额外侧入路视神经管减压术在外伤性失明病人中的应用

目的探讨经额外侧入路视神经管减压术治疗外伤性视神经损伤后失明病人的效果。方法回顾性分析13例外伤性视神经损伤病人(病眼14只)的临床资料,术前病眼视力均为无光感,均采用经额外侧入路视神经管减压术治疗,术后定期随诊。以视力提升2个级别及以上为有效,视力提升1个级别为改善,视力一直无光感为无效。结果术后1周内视力恢复情况:达眼前指数3眼,眼前指动1眼,光感2眼,无光感8眼。术后1个月视力恢复情况:达辨识字体2眼,眼前指数4眼,眼前指动1眼,光感1眼,无光感6眼。远期视力达有效7眼,改善1眼,均在损伤后9 d内行手术治疗;无效6眼,在损伤后9 d内手术2眼,超过9 d行手术治疗4眼。结论外伤性视神经损伤致失明病人保守治疗无改善,应尽快手术治疗,经额外侧入路视神经管减压术是有效的治疗方法。     

Establishing a cat model of acute optic nerve injury

BACKGROUND: In order to investigate the progress in optic nerve injury and the following regeneration and repair, many kinds of animal models of optic nerve injury have been established, such as models of acute and chronic ocular hypertension, compression, amputating wound, ischemia reperfusion or hypoxia, intravitreal injection of excitatory amino acids, etc. However, most of these models are established by squeezing intraorbital optic nerve, and suitable for ophthalmology, and there are fewer models suitable for the acute cranial contusion in neurosurgery. OBJECTIVE: To observe the changes of optic nerve after acute injury, and the characteristics of methods for establishing model of acute optic nerve injury in cats. DESIGN: A complete randomized grouping and controlled animal trial. SETTING: Department of Neurosurgery, General Hospital of Ji’nan Military Area Command of Chinese PLA. MATERIALS: Twenty-eight healthy adult cats, common degree, either sex, weighing 2.0–3.5 kg, were provided by the animal experimental center of Fudan University. The cats were randomly divided into control group (n =3) and model group (n =25), and 5 cats in the model group were observed at 6 hours and 1, 3, 7 and 14 days after injury respectively. JX-2000 biological signal processing system (Department of Physiology, Second Military Medical University of Chinese PLA, Shanghai); Inverted phase contrast microscope (Olympus); Axioplan 2 imaging microgram analytical system (Labsystems). METHODS: The experiments were carried out in the Department of Neurosurgery, General Hospital of Jinan Military Area Command of Chinese PLA from June 2004 to June 2005. The cats in the model groups were made into models of acute optic nerve injury: The cats were anesthetized, then the limbs were fixed in a lateral recumbent position. Pterion approach in human was imitated, the operative incision was made along the line between lateral canthus and tragus, and it could be seen deep along the skull base that white optic nerve (about 3 mm) went through optic foramen and entered into brain tissue. It was squeezed with noninvasive vascular clip for 20 seconds, then the clip was removed, and then the skull was closed after it was examined to be no bleeding. The size of bilateral pupils, direct and indirect light reflexes were observed postoperatively. Successfully established models were judged by larger operated pupil than controlateral one, disappearance of direct light reflex and the existence of indirect light reflex. No model establishment was performed in the control group. Each cat was tested with flash visual evoked potential (F-VEP) to observe the electrophysiological changes before and after experiment. All the cats in the control group and model groups were killed under anesthesia before model establishment and at 6 hours, 1, 3, 7 and 14 days after model establishment respectively, and the pathological changes of the optic nerve after injury were observed under electron microscope and light microscope. MAIN OUTCOME MEASURES: VEP and the ultrastructural changes of optic nerve after acute optic nerve injury in both groups. RESULTS: All the 28 cats were involved in the analysis of results. ① VEP results: The VEP latencies were obviously different between the control group and model group at each time point (P < 0.05), whereas there were no obvious differences among different time points in the model group (P > 0.05). The VEP amplitudes were obviously different between the control group and model group at each time point (P < 0.05), whereas there were no obvious differences among different time points in the model group (P > 0.05). ② Ultrastructural changes of the optic nerve: Under electron microscope, normal optic nerve myelin sheath had complete structure, tramal plates were clear and arranged tightly, axolemma was complete, whereas the structures of endoneurium, myelin sheath, tramal plates, axolemma and axon were in disorders after optic nerve injury. CONCLUSION: Models of acute optic nerve injury established by squeezing intracranial optic nerve with noninvasive vascular clip can be applied in studying intracranial acute optic nerve injury.     

电刺激对大鼠横断视神经视网膜节细胞的影响

目的在建立SD大鼠视神经横断和慢性电刺激模型的基础上,探讨电刺激对视网膜节细胞（RGCs）的保护作用。方法将大鼠随机分成电刺激治疗组和正常对照组,分离暴露右眼视神经并于球后1．5mm处进行横断。电刺激治疗组为分离横断视神经后给予电刺激,正常对照组为横断视神经后给予假性电刺激,在处死前2d断端处放人蘸有5％的荧光金（FG）的明胶海绵,以逆行标记RGCs。在3d、7d、14d不同的时间点处死动物并取材,进行HE染色并用荧光显微镜观察计数视网膜内存活的节细胞。结果在7d、14d电刺激治疗组存活的视网膜神经节细胞数目明显高于正常对照组,差异有显著意义（P〈0．05）。结论电刺激对视神经损伤有一定的保护作用。     

Establishing a cat model of chronic optic nerve compression injury

BACKGROUND:An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved.OBJECTIVE:To establish a stabilized,chronic,optic nerve crush model,which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury.DESIGN,TIME AND SETTING:A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004.MATERIALS:A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT,France;JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA,China;inverted phase contrast microscopy by Olympus,Japan.METHODS:A total of twenty normal adult cats were randomly assigned to control (n = 5) and model (n = 15) groups,according to different doses of contrast agent injected through balloons as follows:0.2 mL injection,0.25 mL injection,and 0.35 mL injection,with each group containing 5 animals.Imitating the clinical pterion approach,the optic nerves were exposed using micro-surgical methods.An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter.Balloon size was controlled with a contrast agent injection (0.1 mL/10 min) to form an occupying lesion model similar to sellar tumors.MAIN OUTCOME MEASURES:The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury.Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy.RESULTS:During the early period (day 11 after modeling),visually evoked potential demonstrated no significant changes.In the late period (day 51 after modeling),recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced.Following injury,the endoneurium,myelin sheath,lamella,axolemma,and axon appeared disordered.CONCLUSION:Results demonstrated that the chronic,intracranial,optical nerve crush model was stable and could simulate optic nerve lesions induced by sellar tumors.Under the condition of chronic optical nerve crush,visually evoked potentials were aggravated.     

猫慢性视神经压迫性损伤模型的构建

BACKGROUND： An animal model of chronic optic nerve injury is necessary to further understand the pathological mechanisms involved. OBJECTIVE： To establish a stabilized, chronic, optic nerve crush model, which is similar to the clinical situation to explore histopathological and optic electrophysiological changes involved in this injury. DESIGN, TIME AND SETTING： A randomized and controlled animal trial was performed at Shanghai Institute of Neurosurgery from May to October 2004, MATERIALS： A BAL3XRAY undetachable balloon and Magic-BD catheter were provided by BLAT, France; JX-2000 biological signal processing system by Second Military Medical University of Chinese PLA, China; inverted phase contrast microscopy by Olympus, Japan. METHODS： A total of twenty normal adult cats were randomly assigned to control （n = 5） and model （n = 15） groups, according to different doses of contrast agent injected through balloons as follows： 0.2 mL injection, 0.25 mL injection, and 0.35 mL injection, with each group containing 5 animals. Imitating the clinical pterion approach, the optic nerves were exposed using micro-surgical methods. An engorged undetachable balloon was implanted beneath the nerve and connected to a catheter. Balloon size was controlled with a contrast agent injection （0.1 mL/10 min） to form an occupying lesion model similar to sellar tumors. MAIN OUTCOME MEASURES： The visually evoked potential examination was used to study optical electrophysiology changes in pre-post chronic optical nerve injury. Ultrastructural pathological changes to the optic nerve were analyzed by electron microscopy. RESULTS： During the early period （day 11 after modeling）, visually evoked potential demonstrated no significant changes. In the late period （day 51 after modeling）, recorded VEP demonstrated that P1 wave latency was prolonged and P1 wave amplitude was obviously reduced. Following injury, the endoneurium, myelin sheath, lamella, axolemma, and axon appeared disordered. CONCLUSION： Results demonstrated that the chronic, intracranial, optical nerve crush model was stable and could simulate optic nerve lesions induced by sellar tumors. Under the condition of chronic optical nerve crush, visually evoked potentials were aggravated.     

依托咪酯促进大鼠视神经损伤后再生的研究

目的探讨依托咪酯对成年大鼠视神经损伤后再生的影响。方法选取25只成年SD大鼠,按随机数字表法随机分为依托咪酯治疗组（腹腔注射依托咪酯脂肪乳注射液,15只）、治疗对照组f腹腔注射脂肪乳,5只）和空白对照组（5只）;治疗组又分为低（2mg／kg）、中（4mg／kg）和高（6mg／kg）剂量3个亚组,每亚组5只。采用自体坐骨神经移植模型和荧光金逆行标记再生视网膜神经节细胞（RGCs）。自体坐骨神经移植术后4周,采用视网膜平铺技术计数再生RGCs。结果空白对照组每张视网膜中再生RGCs数量平均为（1032±147）个,治疗对照组为（1114±179）个,两者之间无明显差异fP〉0．05）。低、中和高剂量依托咪酯治疗组每张视网膜中再生RGCs数量分别为（2054±349）个、（2853±498）个和（4118±615）个,与空白对照组和治疗对照组相比均显著增高（P〈0．01）,而且不同剂量之间均差异显著（P〈0．01）。结论依托咪酯能显著促进大鼠视神经损伤后轴突再生,且具有剂量依赖性。     

猫视神经慢性受压后视网膜神经节细胞的动态观察

目的 观察猫视神经慢性受压后视网膜神经节细胞(RGCs)的动态变化.方法 30只成年家猫按随机数字表法等分为正常对照组、假手术组、压迫1周组、压迫2周组、压迫4周组和压迫8周组,每组5只.利用球囊植入法建立慢性视神经损伤模型.所有动物在术前2周用Dil逆行标记RGCs.取各组动物视网膜进行光镜、电镜观察,并在荧光显微镜下对RGCs进行计数.结果 正常成年猫视网膜HE染色可见三层细胞核,各层间界限较为清楚,从玻璃体腔向巩膜依次为神经节细胞层、双极细胞层和感光细胞层;视神经慢性受压4周时视网膜变化仍不明显:受压8周时可见RGCs核明显稀疏,大而染色浅的细胞核基本消失,视网膜总厚度变薄,胶质细胞增生.电镜下正常猫RGCs核呈卵圆形、核大、核质均匀,有时可见核仁,胞浆占细胞比例小,但细胞器丰富;受压2周时视网膜无明显改变;受压4周和8周时可见RGCs胞浆成分疏松、内质网扩张、线粒体肿胀、质膜下出现空泡、核膜皱缩内陷、胞浆空化、染色质边聚.正常组DiI逆行标记的RGCs的密度在406～527个/mm2之间,平均为(465±38)个/mm2,中央区密度高于周边区;视神经受压后前4周RGCs数量无明显改变;受压8周时RGCs数量有显著下降,平均密度为(293±32)个/mm2.下降约37%.结论 视神经慢性受压后RCJCs将出现延迟的变性.为视神经受压后RGCs的保护提供了时机.     

脑出血大鼠锥体束显微和超微结构改变

目的研究脑出血大鼠锥体束病理变化规律及特点。方法使用Ⅳ型胶原酶．肝素诱导大鼠基底节脑出血,采用劳克坚牢蓝（LFB）染色、神经丝蛋白（NF）免疫组化和电镜对内囊后肢进行观察。结果Ⅳ型胶原酶-肝素能成功建立具有典型神经功能缺损的大鼠脑出血模型。光镜发现锥体束髓鞘损伤在脑出血1～3d逐渐加重,7d开始再生修复,1～7d轴突损伤持续加重,14d轴突光度值（0．09±0．01）有所增加,但与7d（0．10±0．02）相比无显著性差异（P〉0．05）。电镜显示脑出血1d锥体束髓鞘松解,轴突水肿,部分无髓轴突崩解坏死消失,3d髓鞘松解、空泡样变性,局部髓鞘消失、厚薄不均,轴突水肿严重,甚至坏死崩解。结论大鼠脑出血后1w内锥体束损伤呈进行性加重,提示应早期和超早期予以干预治疗以减轻损伤和促进修复。     

嗅神经鞘细胞和自体坐骨神经移植修复受损视神经

背景：有研究已初步证明了甲泼尼龙对受损视网膜节细胞的早期保护作用。 目的：观察甲泼尼龙联合嗅神经鞘细胞和自体坐骨神经移植大鼠受损视神经纤维及其髓鞘的形态学及计数变化。 设计、时间及地点：随机对照动物实验，于2005-09/2006-03于北京大学医学部神经解剖实验室完成。 材料：选取成年雄性SD大鼠40只，取其中4只做形态学正常对照。 方法：其余36只大鼠按随机数字表法分为6组，即视神经损伤模型组、甲泼尼龙组、嗅神经鞘细胞移植组、嗅神经鞘细胞移植+甲泼尼龙组、坐骨神经移植组、坐骨神经移植+甲泼尼龙组，每组6只。 主要观察指标：取视神经，制作冰冻切片，移植后14，21 d分别从各组切片中随机抽取10张载玻片，对生物素标记的葡聚糖胺染色的视神经纤维及甲苯胺蓝染色的视神经髓鞘进行形态学观察，电镜下对视神经纤维髓鞘进行计数。 结果：顺行追踪剂生物素标记的葡聚糖胺在视神经中的染色结果主要表现为嗅神经鞘细胞移植+甲泼尼龙组、坐骨神经移植+甲泼尼龙组，与视神经损伤模型组相比，神经纤维排列较整齐，发生中晚期溃变的纤维比例较小。移植后14，21 d，甲泼尼龙组视神经纤维髓鞘数量均显著高于视神经损伤模型组(P < 0.05，0.01)。坐骨神经移植+甲泼尼龙组均显著高于坐骨神经移植组(P < 0.05)。嗅神经鞘细胞移植+甲泼尼龙组均显著高于嗅神经鞘细胞移植组(P < 0.05)。 结论：形态学结果表明嗅神经鞘细胞和自体坐骨神经移植与甲泼尼龙的联合作用能激发并增强受损中枢神经的自我保护及修复作用，对视神经纤维及其髓鞘溃变速度有延缓作用。     

三重脑震荡鼠模型建立及组织病理学动态改变观察

目的建立三重脑震荡（MCC）大鼠模型,观察MCC鼠不同结构神经元及轴索的病理学变化,探索运动员多次脑震荡损伤机制。方法用金属单摆闭合性脑损伤打击装置复制大鼠MCC模型48只,随机分为1、2、4、8、16和24d组（n=8）。另设正常对照组（n=8）。定时戊巴比妥钠麻醉,4％多聚甲醛心腔灌注处死,取脑。用Nissl染色、Bielschowsky银染和Weil髓鞘染色显示神经元、轴索和髓鞘,对固缩变性神经元数目、轴索直径和髓鞘变性进行半定量分析。结果伤后：①1～24d皮层、海马和脑干网状结构神经元不同程度固缩变性,以2d组为重;②轴索不同程度的肿胀、变形、排列紊乱、收缩球形成;轴索直径平均值均大于对照组,以2、4d组最为明显（P〈0．05）;③髓鞘肿胀、淡染,灰度值增高,与对照组相比,1～16d组均有统计学意义（P〈0．05）。结论大鼠MCC后,脑神经元出现不同程度弥漫性的固缩变性,轴索肿胀、髓鞘淡染的病理改变。