腦水腫的發病機理及藥物治療醫院及講者信息腦水腫腦實質聚集過量液體腦水腫分類血管源性腦水腫血腦屏障受損所致，大量液體和血管內蛋白質積聚于腦白質細胞間隙常見于腦創傷、腦出血、腦缺血的第二階段腦水腫動物實驗模型凍傷模型液壓沖擊傷模型腦出血模型水中毒模型肝損模型TheColdInjuryModelColdinjuryisperformedbyinflictingfreezestimulationonthehemisphereoftheskulloftheanimalAftercoldinjury,BBBdisruptionisindicatedbyevaluatingextravasationofEvansbluedye凍傷模型主要用于血管源性腦水腫的試驗模型凍傷直接破壞血管細胞，導致不可逆的血腦屏障損傷特點：試驗的可重復性及受傷面積的準確性TheFluidPercussionInjury(FPI)ModelFluidpercussioninjuryisperformedbyaninjurytotheintactduraaftercraniectomybyimpactsofrapidlypushedfluid(B1,B2).Aswellascoldinjury,theextravasationofEvansbluedyeisobserved(B3).液壓沖擊傷模型模擬腦創傷引發的腦水腫可誘導各種降解酶如MMP-9的激活，導致血管基底膜的降解可觀察到炎性介質的增加及巨噬細胞的浸潤；TheCerebralHemorrhageModel通過腦實質內注射膠原蛋白酶破壞血管基底膜或者注射自體血制備腦出血模型（ICHmodel）常見的蛛網膜下腔出血模型（SAHmodel）包括：單側出血、雙側出血、血管內穿刺模型可同時觀察到血管源性腦水腫及細胞毒性腦水腫BBBbreakdownBBBdysfunctionthrombinandhemoglobinextravasationinflammatoryresponsesTheLiverFailureModel急性或慢性肝細胞失功引發的肝衰會誘導肝性腦病，造成中樞神經組織嚴重失功。急、慢性肝衰導致的腦水腫發病機制不同急性肝衰，ICP上升；慢性肝衰很少觀察到ICP上升肝衰模型產生的腦水腫為細胞毒性腦水腫星形細胞腫脹血腦屏障未見損害一般采用硫代乙酰胺誘導肝細胞損傷氨基半乳糖誘導急性肝衰膽管結扎或門腔靜脈吻合術誘導慢性肝衰Wet-DryWeightMethodacommonandsimplemethodinvasiveandnotperformedinpatientsbasedontheweightmeasurementofbraintissuebeforeandaftercompletedehydrationWatercontent(%)=100×(wetweight?dryweight)/wetweightWatercontent=(wetweight?dryweight)/dryweightTissueswelling(%)=100×

(finalwetweight?initialwetweight)/initialwetweightwetweight：Theweightbeforedehydrationdryweight：theweightafterdehydrationMagneticResonanceImaging(MRI)anoninvasivemethod，usedforevaluatingbrainedemainpatientsandexperimentalanimalsTwoIndex:apparentdiffusioncoefficient（ADC）reducedADCvaluescorrelatewithcytotoxicedemaT2imagingtheincreasedT2valuesreflectthedevelopmentofvasogenicedema腦水腫關鍵因子及治療VEGF、MMPs、AQPs、NKCC1、ETB-R、GR腦水腫生成關鍵因子抗水腫治療藥物作用靶點藥物分類抗水腫類型VEGFVEGF抑制劑；VEGF受體拮抗劑；血管源性腦水腫MMPsMMPs抑制劑；血管源性腦水腫AQPsAQ4抑制劑；AQ4激動劑細胞毒性腦水腫血管源性腦水腫NKCC1Bumetanide（布美他尼）細胞毒性腦水腫SUR1-regulatedNCCa-ATPGlibenclamide格列本脲細胞毒性腦水腫ETB-RETB-R拮抗劑血管源性腦水腫糖皮質激素受體地塞米松七葉皂苷鈉血管源性腦水腫麥通納作用機制作用與GCR/NF?κB

信號通路，抗炎作用上調GC受體表達，抑制NF?κB的活化1,2抑制TNF-α,IL-1β等炎癥因子的產生3封閉毛細血管，減少毛細血管壁上小孔的數量和直徑4維持正常血管通透性抑制局部炎癥細胞滲出提高SOD活性，清除氧自由基51，EXPERIMENTALANDTHERAPEUTICMEDICINE6:419-422,20132，MolPharmacol.2010May;77(5):818-273，JZhejiangUnivSciB.2005Jan;6(1):28-324，Arzneimittelforschung.1970May;20(5):699-7035，YaoXueXueBao.2004Jun;39(6):419-23.麥通納協同激素抗炎消腫低劑量可的松、麥通納聯合給藥6h，水腫顯著減輕N.Jiangetal./Phytomedicine18(201