侧脑室脑脊液冲击能量对室周结构创伤的动物模型
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摘要
目的：研制侧脑室脑脊液对室周结构撞击所致脑损伤的动物模型，观察在这个模型不同的分级能量撞击下，动物脑室周诸结构的病理改变，光镜、电镜下的形态学改变及动物的多种病理生理学变化；方法：新西兰兔64只，分为对照组(8只)、假手术组(8只)及轻伤组(16只)：撞击能量为0.23焦耳；中伤组(16只)撞击能量为0.52焦耳；重伤组(16只)撞击能量为0.92焦耳；参考胡学强等的方法行右侧脑室额角置管；各组动物于不同时间点(1、2、8、24、48、72小时)杀死取材，分别测定脑水含量、HE及B-APP染色后之光镜下改变、电镜下神经元及轴索的超微结构的改变。结果：1轻、中、重伤组死亡率分别为6.25％、18.70％、50％(三组比较P＜0.05)，对照组及假手术组无死亡。2撞击后，动物均出现明显的脑室损伤反应，包括损伤后即刻血压骤升后骤降，呼吸更深快及呼吸骤停，其中重伤组反应最剧烈。3轻、中、重伤组伤后意识恢复时间比较存在显著性差异(分别为2.11±0.40h、5.85±1.23h、7.83±0.40hP＜0.05)。4免疫切片显示：各损伤组兔脑多个部位(海马、胼胝体、丘脑、脑干等)显著广泛性轴索损伤改变。5电镜显示脑室周结构轴突内微管减少甚至消失，神经丝排列紊乱，被覆髓鞘出血片层分离及突出，脉络膜上皮细胞固缩坏死，绒毛消失。结论：侧脑室内脑脊液一定能量的冲击可以造成室周结构的明显损伤，且撞击能量越大，损伤程度越重。故在考虑减速性脑损伤时，脑室液对室周结构的撞击力不应被忽略。本模型复制出了动物脑外伤后较长时间的持续昏迷，结合丘脑和脑干处的病理改变，认为丘脑在重度脑外伤后的持续昏迷中扮演了重要的角色；脑干、海马区的病理变化对临床上脑震荡患者短暂意识障碍及伤后的记忆障碍均可从神经解剖上进行解释。胼胝体区大量轴索损伤的改变至少说明在发生DAI时并非只有外力的传导，其中脑室液对侧脑室顶(胼胝体)的撞击完全有可能是造成DAI时胼胝体大量轴索损伤。伤后脉络丛的病理改变可以解释部分脑外伤患者伤后出现的原发性脑室内出血的原因。本模型简单、经济、可分级、重复性好。
Objective: To set up an experimental animal model of head injuryresulting of ventricular cerebrospinal fluid impacting the periventriclularstructure. Furthermore, to investigate the pathological changes, themorphological changes under light microscope and electron microscopeand the pathophysiological changes of each animal body, which arerelating to different power of impact. Methods: 64 rabbits were dividedinto 5 groups, including control group (n=8), sham operation group (n=8),mild injury group (n=16), moderate injury group (n=16) and severe injurygroup (n=16). Each injury group received the power of impact as 0.23 J,0.52 J and 0.92 J individually. All the groups of rabbits were killed atdifferent times(1h, 2h, 8h, 24h, 48h,72h) after impact. Each wereexamined the content of brain water and the ultrastructural changes undermicroscope. Results: 1. The mortality of each injury group were 6.25%、18.70%、50% respectively (P＜0.05), while no death was found in controlgroup and sham operation group. 2. The physiological responses afterimpact were observed in all traumatic animals, which showed a suddenrise or reduction of blood pressure, deep and fast breath and apnea, et al.The responses were the most obvious in the severe injury group. 3. Therecovery time was significantly different in each injury grouprespectively (2.11±0.40h, 5.85±1.23h, 7.83±0.40h, P＜0.05). 4.Immunohistological examination showed that the diffuse axonal injury(DAI) could be seen in several parts of the brain (hippocampus,thalamencephal, corpus callosum, brain stem). 5. The electronmicroscope showed reduction or disappearance of microtubule in axons,microfilaments ranging disorderly, medullary sheath bleeding, pyknosisof chorioidal epithelium cells. Conclusion: The impact power acquiredby ventricular fluid during decelaration can damage the periventriclularstructure and produce a series of physiopathologic changes. In addition,the greater power of the impact, the more serious injury of the structure.This model succeeded in keeping the animal in coma for a long time. Thepathologic changes of thalamencephal and the brainstem reached for sucha conclusion that the thalamencephal may play an important role in keeping the animal in coma for a long time after severe injury. Based onthe knowledge of nerve's anatomy, the pathologic changes of thebrainstem and the hippocampus can explain the transient consciousdisturbance in patients with cerebral concussion and the dysmnesia afterinjury. The DAI in the corpus callosum demonstrated that not only theconduction of outside strength but also the impact of ventricular fluidboth participate in DAI. The pathologic changes of the choroid plexus canpartly explain the primary intraventficular hemorrhage after injury. Thismodel is simple and cheap, and has a good ability of classifying andrepeating.
Objective: To set up an experimental animal model of head injuryresulting of ventricular cerebrospinal fluid impacting the periventriclularstructure. Furthermore, to investigate the pathological changes, themorphological changes under light microscope and electron microscopeand the pathophysiological changes of each animal body, which arerelating to different power of impact. Methods: 64 rabbits were dividedinto 5 groups, including control group (n=8), sham operation group (n=8),mild injury group (n=16), moderate injury group (n=16) and severe injurygroup (n=16). Each injury group received the power of impact as 0.23 J,0.52 J and 0.92 J individually. All the groups of rabbits were killed atdifferent times(1h, 2h, 8h, 24h, 48h,72h) after impact. Each wereexamined the content of brain water and the ultrastructural changes undermicroscope. Results: 1. The mortality of each injury group were 6.25%、18.70%、50% respectively (P＜0.05), while no death was found in controlgroup and sham operation group. 2. The physiological responses afterimpact were observed in all traumatic animals, which showed a suddenrise or reduction of blood pressure, deep and fast breath and apnea, et al.The responses were the most obvious in the severe injury group. 3. Therecovery time was significantly different in each injury grouprespectively (2.11±0.40h, 5.85±1.23h, 7.83±0.40h, P＜0.05). 4.Immunohistological examination showed that the diffuse axonal injury(DAI) could be seen in several parts of the brain (hippocampus,thalamencephal, corpus callosum, brain stem). 5. The electronmicroscope showed reduction or disappearance of microtubule in axons,microfilaments ranging disorderly, medullary sheath bleeding, pyknosisof chorioidal epithelium cells. Conclusion: The impact power acquiredby ventricular fluid during decelaration can damage the periventriclularstructure and produce a series of physiopathologic changes. In addition,the greater power of the impact, the more serious injury of the structure.This model succeeded in keeping the animal in coma for a long time. Thepathologic changes of thalamencephal and the brainstem reached for sucha conclusion that the thalamencephal may play an important role in keeping the animal in coma for a long time after severe injury. Based onthe knowledge of nerve's anatomy, the pathologic changes of thebrainstem and the hippocampus can explain the transient consciousdisturbance in patients with cerebral concussion and the dysmnesia afterinjury. The DAI in the corpus callosum demonstrated that not only theconduction of outside strength but also the impact of ventricular fluidboth participate in DAI. The pathologic changes of the choroid plexus canpartly explain the primary intraventficular hemorrhage after injury. Thismodel is simple and cheap, and has a good ability of classifying andrepeating.
引文
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