《中国康复理论与实践》

《中国康复理论与实践》 ›› 2009, Vol. 15 ›› Issue (09): 807-809.

• 专题 • 上一篇    下一篇

孕鼠腹腔注射脂多糖合并缺氧环境造成宫内胎鼠脑部损伤

陈刚1a;胡燕荣1b;钟杰2;刘伟1a;李江1a;温林豹1a;李建新1c;杨小朋1a;朱沂1c;孙振柱1d   

  1. 1.新疆维吾尔自治区人民医院，a神经外科;b.皮肤病研究所;c.神经内科;d.病理科,新疆乌鲁木齐市 830001;2.乌鲁木齐市友谊医院神经外科，新疆乌鲁木齐市 830000
  • 收稿日期:2009-06-12 修回日期:2009-07-28 出版日期:2009-09-01 发布日期:2009-09-01

Periventricular Leukomalacia Induced by Prenatal Exposure to Lipopolysaccharide Followed Perinatal Hypoxic Insults: An Animal Model for Perinatally Acquired Encephalopathy

CHEN Gang,HU Yan-rong,ZHONG Jie,et al   

  1. Departmet of Neurosurgery, Xinjiang Uygur Autonomous Region People's Hospital, Urumqi 830001, Xinjiang, China
  • Received:2009-06-12 Revised:2009-07-28 Published:2009-09-01 Online:2009-09-01

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摘要： 目的 探讨孕鼠宫内感染合并缺氧致幼鼠脑瘫的模型制作及评价方法。方法 实验动物分为3组：脂多糖缺氧组:健康Wistar孕鼠脂多糖腹腔注射，12 h后置于缺氧环境中2.5 h，4 h后再次腹腔注射脂多糖；颈动脉结扎缺氧组：7 d龄Wistar幼鼠结扎右侧颈动脉结合缺氧环境；对照组：7 d龄Wistar幼鼠仅行颈正中切口。于术后4周行足印分析试验、股四头肌复合肌肉动作电位（CMAP）及病理学检测。结果 与对照组相比，脂多糖缺氧组和颈动脉结扎缺氧组前后肢足印重复性差，表现为间距较大，且间距不稳定（P<0.05）；CMAP引出最大波幅所需的刺激强度增大，引出波幅降低（P<0.05）； 脑室旁正常组织结构破坏，细胞排列紊乱，局部大小不等圆形软化灶；胞浆内容物缺失，部分核膜破损，核内容物外溢。结论 应用孕鼠宫内感染合并缺氧的方法制作幼鼠脑瘫模型稳定可靠，与单侧颈动脉结扎缺氧模型相比具有微创、简单易行、更逼真地模拟人类在怀孕晚期宫内感染缺氧致胎儿脑部损伤的优点。

关键词: 脑性瘫痪, 脂多糖, 炎症, 缺血缺氧, 动物模型, 大鼠

Abstract: Objective To establish a new rat model of perinatal brain damage. Methods Wistar rats were randomized into 3 groups: lipopolysaccharide （LPS） plus hypoxia (H) group: 17 d pregnant rats exposure in utero to LPS followed by hypoxia; hypoxia (H)/ ischemia (I) group: postnatal day 7 (P7) pups ligated the right common carotid artery followed by exposure to hypoxia (8% O2 ) for 2 h; control group: P7 pups incised the anteriorl cervical skin only. The footprint analysis, compound muscle action potential (CMAP) and pathological observation were performed after 4 weeks. Results The left limb footprint repeatability of rat in HI and LPS plus H groups was poorer than that in control group （P<0.05）. The hindlimb quadriceps CMAP of rats in HI and LPS plus H groups showed that the wave amplitude was lower than that in control group （P<0.05）. The periventricular cells were irregular, and the periventricular leukomalacia was seen. The morphous of the neurocytes was irregular obviously, part of the nuclear membranes was broken down with the content leakage under transmission electron microscope. Conclusion The animal model for cerebral palsy has established, that mimics more the occurrence of this disease in human.

Key words: cerebral palsy, lipopolysaccharide, inflammation, hypoxia-ischemia, animal model, rats