血管源性脑水肿

其中血管源性脑水肿发生以血脑屏障（BBB）通透性的改变为主要原因。

The major cause of vasogenic cerebral edema is the change of blood-brain barrier ( BBB ) permeability .

碱性磷酸酶单克隆抗体对大鼠血管源性脑水肿的治疗作用

Therapeutic role on monoclonal antibody of alkaline phosphatase to vasogenic cerebral edema in rats

实验性大鼠急性期脑缺血血脑屏障开放、血管源性脑水肿MRI与脑组织MMP-9、VEGF表达

Blood-brain Barrier Opening and Vasogenic Brain Edema of Experimental Acute Ischemia of Rats : MRI Evaluation , and the Correlation with MMP-9 and VEGF Expression in Infarcted Brain Tissue

血管源性脑水肿（vasogenicbrainedema，VBE）是脑缺血后的重要病理生理变化，可加重因缺血缺氧而引起的神经细胞损伤。

Vasogenic brain edema ( VBE ) is very important pathological change after cerebral ischemia , which can aggravate the ischemic damage .

【结论】外伤后2hNF能加重血管源性脑水肿，但能改善细胞毒性脑水肿，而在24h能改善血管源性脑水肿。

[ Conclusion ] NF could aggravate the vasogenic brain edema but alleviate cytotoxic brain edema at 2 hr after insult and could alleviate cytogenous brain edema at 24 hr .

酶屏障抑制剂951治疗血管源性脑水肿

Treatment of Vasogenic Brain Edema with Inhibitor 951 of Enzyme Barrier

活血化瘀药对大鼠脑缺血再灌注血管源性脑水肿的影响

Influence of blood-activating and stasis-eliminating drugs on angiogenic cerebral edema of rats after cerebral ischemia-reperfusion

大鼠血管源性脑水肿模型3TMR弥散成像动态研究

Vasogenic Brain Edema Model of Rats : A Series Study of 3T MR Diffusion Imaging

目的：从酶屏障的角度观察乳酸脱氢酶抗体对大鼠血管源性脑水肿的干预作用。

AIM To observe the interventional effect of lactate dehydrogenase antibody on vasogenic brain edema in rats .

模型制备及给药：用腹腔注射苯肾上腺素的方法制成血管源性脑水肿模型。

Model establishment and administration Models of vasogenic brain edema were made by intraperitoneal injection of phenylephrine .

[结论]1,2-二氯乙烷可造成血脑屏障细胞的损伤，引起血管源性脑水肿。

[ Conclusion ] 1 , 2-dichloroethane can damage blood-brain barrier cells , and induce cerebral edema .

血脑屏障通透性增高是造成血管源性脑水肿和炎症反应等病理学变化的主要环节。

Hypoxia may usually cause an increase in blood-brain barrier ( BBB ) permeability , resulting in vasogenic brain edema and aggravating neuronal injury .

目的：探讨预防性应用活血化瘀药对大鼠脑缺血&再灌注所致血管源性脑水肿的作用。

AIM : To discuss the effects of blood activating and stasis eliminating drugs on angiogenic cerebral edema of the rats following cerebral ischemia reperfusion .

乳酸脱氢酶抗体对减少血管源性脑水肿大鼠脑灰、白质水分含量、降低血脑屏障通透性均有显著效果。

Lactate dehydrogenase antibody has significant effect in reducing the water content in the gray matter and white matter and decreasing BBB permeability of rats with vasogenic brain edema .

超微结构提示在缺血60分钟时有细胞毒性脑水肿存在，当再灌流120分钟时，细胞毒性和血管源性脑水肿同时存在。

The ultrastructure revealed that cytotoxic brain edema was present at 60 minutes of ischemia , and both cytotoxic and vasogenic brain edema occurred after 120 minutes of reperfusion .

目前对于脑水肿的研究表明，血管源性脑水肿和细胞毒性脑水肿是主要的发病机制，这两种发病机制同时参与肝硬化时脑水肿的形成过程。

Current studies in cerebral edema shows the two main pathogenesis of brain edema is vasogenic and cytotoxic cerebral edema , which participate in the formation of cerebral edema simultaneously .

结论：活血化瘀药能减少缺血再灌注大鼠脑的一氧化氮产生，降低血管源性脑水肿的程度，减轻神经细胞损伤，具有抗缺血再灌注损伤作用。

CONCLUSION : The blood activating and stasis eliminating drugs can inhibit the produce of NO in the brain of ischemia reperfusion rats , relieve the severity of angiogenic cerebral edema , alleviate the nerve cell damage and protect rats against ischemia reperfusion injury .

结论严重烧伤早期脑水肿模型兼有血管源性和细胞毒性脑水肿的MRI及病理组织学特征。

Conclusion The model of the brain edema after severe burn had the feature of both vasogenic edema and cellular edema in the MRI and pathology .

目的探讨一氧化氮（NO）与脑胶质瘤血管形成、瘤周血管源性脑水肿的关系。

Objective To investigate the relationship between NO and angiogenesis and peritumorous brain edema of gliomas .

多数研究认定，高原性脑水肿主要是血-脑屏障功能和结构的障碍，导致血管通透性增高，形成血管源性脑水肿，并且伴有细胞毒性脑水肿。

Most researches have proved that high altitude cerebral edema is mainly the blood brain barrier , function and structure barrier , which leads to the increasing of vascular permeability and forms vasogenic brain edema along with cytotoxic brain edema .

恢复缺血部位的血供确实是治疗脑缺血疾病的一个关键所在，但是缺血再灌也有可能导致脑微血管损害，出现血管源性脑出血、脑水肿，加重脑损害。

For sure the reperfusion of ischemia part is one of the keys to cure CVD , but reperfusion maybe injure the microvascular , lead to cerebral hemorrhage , hydrocephalus , aggravate brain damage .