鼠脑液压伤后血脑屏障通透性变化对磷脂酶A_2和脑水肿的影响  

Changes in bloodbrain barrier permeability,phospholipase A2,water contents in rats after brain injury

作　　者：刘海东[1,2] 王文仲[1,2] 周晓平[1,2] 陈思峰[1,2] 方健 

机构地区：[1]第二军医大学长海医院 [2]第二军医大学病理生理教研室

出　　处：《中国危重病急救医学》1998年第6期326-328,共3页Chinese Critical Care Medicine

基　　金：全军临床医学中青年人才培养基金

摘　　要：目的：研究颅脑损伤早期血脑屏障通透性（ＢＢＢＰ）、磷脂酶Ａ２（ＰＬＡ２）与脑水肿的改变及其相关关系；以及地塞米松和尼莫地平治疗的影响。方法：应用鼠脑液压伤模型，观测伤后不同时间伊文氏蓝在伤侧脑组织内吸光度变化、ＰＬＡ２和脑含水量改变；并观测经腹腔注射地塞米松和尼莫地平后上述指标的改变。结果：液压伤后１小时伤侧脑组织伊文氏蓝吸光度开始升高，伤后６小时至峰值，随后逐渐降低，伤后１２小时～７２小时仍维持在高于对照组１倍以上的水平；ＰＬＡ２于液压伤后１小时发生改变，１２小时～２４小时达峰值，４８小时～７２小时仍高于对照组；脑含水量在伤后２４小时～７２小时呈阶梯状升高；创伤早期ＢＢＢＰ的改变程度较ＰＬＡ２和脑含水量明显；ＢＢＢＰ与ＰＬＡ２和脑含水量均呈正相关。结论：①创伤早期ＢＢＢＰ增加是由脑血管功能紊乱和机械物理损伤所致，也是ＰＬＡ２升高和血管源性脑水肿形成的诱因；②创伤后２４小时～７２小时ＰＬＡ２的升高，导致细胞毒性脑水肿，促使血脑屏障结构破坏，ＢＢＢＰ增加，脑继发性损伤加重，３者间呈互相增强作用；③早期应用大剂量地塞米松和尼莫地平治疗对抑制ＰＬＡ２的活性。Objective:To investigate changes in bloodbrain barrier permeability(BBBP),phospholipase A2(PLA2),and water contents and the treatment effect with dexamethasone (DXM) and nimodepine (NIMO) on brain injury in rats.Methods:Ninety rats were divided into 9 groups (10 animals in each group).By using a rat model of fluid percussion injury to brain,light absorbed density of Evan′s blue,PLA2 activity and water content in the cerebrum on the injured side were determined.The effect of treatment with DXM and NIMO were also observed in this study.Results:The light absorbed density of Evan′s blue began to increase an hour after injury,peaking at 6 hours and decreasing thereafter (all P<001).Similarly,PLA2 activity elevated an hour after the injury (P<001),peaking at 12 to 24 hours,and it was still higher than that of the controls at 48 to 72 hours (all P<001).Meanwhile,water content in the cerebrum persistently increased at 24 to 72 hours (all P<001).In addition,changes in BBBP were greater than those in PLA2 and water content of the cerebrum during early stage after brain injury,and positive correlations were found between BBBP and PLA2 or water content.Conclusions:①The elevation of BBBP may be associated with cerebral vascular dysfunction and mechanical physical injury,resulting in PLA2 release and cerebral edema.②The increase of PLA2 would give rise to cytotoxic cerebral edema,thereby leading to damage of the bloodbrain barrier and high BBBP.③Additionally,treatment with DXM and NIMO has significant effects on inhibiting PLA2 activity and reducing BBBP as well as cerebral edema at the early stage following acute brain injury.

关 键 词：脑液压伤模型 磷脂酶A2 血脑屏障通透性 脑水肿 

分 类 号：R651.15[医药卫生—外科学]