›› 2010, Vol. 30 ›› Issue (9): 1106-.doi: 10.3969/j.issn.1674-8115.2010.09.021

• 论著(基础研究) • 上一篇    下一篇

小型猪脑外伤急性颅内高压并失血性休克模型的建立

罗 伟1, 李雪元2, 李 甲2, 渠兴乾1, 陈李骏1, 沈伯雄1, 冯东福2   

  1. 上海交通大学 医学院附属第三人民医院 1.麻醉科, 2.神经外科 创伤医学研究所, 上海 201900
  • 出版日期:2010-09-25 发布日期:2010-09-27
  • 通讯作者: 冯东福, 电子信箱: dffeng@21cn.com。
  • 作者简介:罗 伟(1970—), 男, 副主任医师, 硕士;电子信箱: lowi126@126.com。
  • 基金资助:

    上海市科委基金(064119639)和上海交通大学医学院附属第三人民医院基金(syz09-12)

Miniature pig model of combined traumatic brain injury and acute intracranial hypertension with hemorrhagic shock

LUO Wei1, LI Xue-yuan2, LI Jia2, QU Xing-qian1, CHEN Li-jun1, SHEN Bo-xiong1, FENG Dong-fu2   

  1. 1.Department of Anesthesiology, 2.Department of Neurosurgery, Institute of Traumatic Medicine, The Third People's Hospital, Shanghai Jiaotong University School of Medicine, Shanghai 201900, China
  • Online:2010-09-25 Published:2010-09-27
  • Supported by:

    Shanghai Science and Technology Committee Foundation, 064119639;Foundation of The Third People's Hospital, Shanghai Jiaotong University School of Medicine, syz09-12

摘要:

目的 建立小型猪脑外伤急性颅内高压并失血性休克模型,模拟多发伤失血性休克合并脑外伤急性硬膜外血肿,分析其形态学改变。方法 对16只实验用小型猪,采用简易脑皮层气击装置致伤一侧脑额叶,硬膜外球囊法致急性颅内高压,改良Wigger 氏休克模型法致失血性休克。观察模型制备前(T01)及放血完成后即刻(T0)、15 min(T15)、30 min(T30)、60 min(T60)五个时间点的平均动脉压(MAP)、颅内压(ICP)和脑灌注压(CPP);于T01和T60两个时间点测颈静脉血氧饱和度(SjvO2)。随机选取2只动物,于模型制备前和制备后6 h分别行头颅冠状位CT和MRI检查。模型制备后6 h,随机选取2只动物分别行脑大体病理、HE染色观察和超微结构观察。结果 与T01时间点比较,T0时间点MAP和CPP明显下降,ICP明显升高,差异均有统计学意义(P<0.05);与T0时间点比较,T15、T30和T60时间点的MAP、ICP和CCP无明显变化(P>0.05)。T60时间点SjvO2较T01时间点明显下降(P<0.05)。影像学检查发现,创伤性硬膜下出血,中线偏移,对侧脑室扩张。HE染色观察发现,创伤灶及周围脑组织水肿明显,炎症细胞浸润,毛细血管周隙出血,白质区淤点性出血以及灰质挫裂伤。超微结构观察显示,创伤灶、周围和对侧脑组织表现为严重程度递减的改变,包括神经元坏死、变性,轴索脱髓鞘,线粒体肿胀,内皮细胞水肿等形态改变。结论 采用控制性脑皮层冲击、硬膜外球囊及股动脉放血方法建立的小型猪脑外伤急性颅内高压并失血性休克组合模型,可模拟临床多发伤失血性休克并脑外伤急性硬膜外血肿,并能用于CPP和脑氧供需平衡的监测。

关键词: 创伤性脑损伤, 颅内高压, 失血性休克, 颈静脉血氧饱和度, 动物模型, 小型猪

Abstract:

Objective To establish the miniature pig model of combined traumatic brain injury and acute intracranial hypertension with superimposed hemorrhagic shock so as to simulate the human local traumatic brain injury and acute epidural hematoma and superimposed hemorrhagic shock, and analyse the morphological changes. Methods Unilateral brain frontal lobes were injured by simplified controlled cortical impact devices in 16 miniature pigs, epidural balloon method was adopted to induce acute intracranial hypertension, and modified Wigger shock model was employed to cause hemorrhagic shock. Mean arterial blood pressure (MAP), intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were observed at the time points of before model preparation (T01), immediately after blood withdrawal (T0), and 15 min (T15), 30 min (T30) and 60 min (T60) after blood withdrawl. O2 suturation of jugular venous blood (SjvO2) was monitored at T01 and T60. Two miniature pigs were randomly selected, and cranial CT and MRI examinations at coronal plane were performed before model preparation and 6 h after model preparation. Two miniature pigs were randomly selected 6 h after model establishment for cranial gross pathological examination, observation with HE staining and ultramicrostructure observation. Results MAP and CPP were significantly lower and ICP was significantly higher at T0 than those at T01 (P<0.05). There was no significant difference between MAP, ICP and CCP of T15, T30 and T60 and those of T0 (P>0.05). SjvO2 at T60 was significantly lower than that at T01 (P<0.05). Imaging examinations revealed traumatic subdural hemorrhage, midline shift and contralateral cerebral ventricle dilation. It was observed by HE staining that there were significant edema in traumatic lesions and adjacent tissues, infiltration of inflammatory cells, pericapillary hemorrhage, petechial hemorrhages in the white matter and cortical laceration. Ultramicrostructure observation revealed a series of changes in the tissues of traumatic lesions, adjacent tissues and contralateral cerebral tissues, including necrosis and degeneration of neurons, myelinolysis of axons, mitochondrial swelling and distension of endothelia. Conclusion The miniature pig model of traumatic brain injury combined with acute intracranial hypertension and hemorrhagic shock, established successfully with controlled cortical impact, epidural balloon and blood withdrawal, can effectively simulate human local traumatic brain injury and acute epidural hematoma and superimposed hemorrhagic shock, and can monitor the cerebral perfusion and balance of supply and demand of cerebral oxygen.

Key words: traumatic brain injury, intracranial hypertension, hemorrhagic shock, O2 suturation of jugular venous blood, animal model, miniature pigs