机构地区:[1]Department of Neurosurgery, General Hospital of Jinan Military Area Command of Chinese PLA, Jinan 250031, Shandong Province, China [2]Department of Neurosurgery, Changzheng Hospital, Second Military Medical University of Chinese PLA, Shanghai 200003, China
出 处:《Neural Regeneration Research》2009年第6期462-467,共6页中国神经再生研究(英文版)
基 金:the National Natural Science Foundation of China,No.30271333
摘 要: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 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
关 键 词:optic nerve injury evoked potential visual sensation FELINE disease models animal
分 类 号:R338[医药卫生—人体生理学]
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