Blood-brain barrier pathophysiology and ischaemic brain oedema
Blood-brain barrier pathophysiology and ischaemic brain oedema
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DOI：
10.1016/s0750-7658(03)00069-8
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发表时间：
2003-04-01
影响因子：
--
通讯作者：
Copin, JC
中科院分区：
文献类型：
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作者：
Gasche, Y;Copin, JC
脑水肿是脑梗塞的潜在致命并发症。缺血通过改变膜离子泵功能诱导细胞肿胀和细胞毒性水肿。它还启动早期氧化和炎症级联反应，导致血脑屏障破坏、血管源性水肿和出血性转化。血脑屏障破坏的机制涉及内皮细胞活化和基质金属蛋白酶引起的内皮基底膜降解。组织纤溶酶原激活剂再灌注是改善中风预后的唯一治疗方法。这种治疗还会增加血管源性水肿和症状性出血转化的风险，从而降低再灌注的益处。实验研究表明，抑制血脑屏障蛋白水解可减少血管源性水肿和出血风险。最近在理解缺血期间血脑屏障破坏方面取得的进展提出了新的治疗策略，使用能够干扰缺血级联的药物，以增加缺血发作和溶栓再灌注之间的治疗窗口。 (C) 2003 年科学与医学版 Elsevier SAS。全部的权力储备。
Cerebral oedema is a potentially lethal complication of brain infarction. Ischemia, by altering membrane ionic pump function, induces cell swelling and cytotoxic oedema. It also initiates early oxidative and inflammatory cascades leading to blood-brain barrier disruption, vasogenic oedema and haemorrhagic transformation. The mechanisms of blood-brain barrier disruption involve endothelial cell activation and endothelial basal membrane degradation by matrix metalloproteinases. Reperfusion by tissue plasminogen activators is the only treatment improving stroke prognosis. This treatment also increases vasogenic oedema and the risk of symptomatic haemorrhagic transformation, reducing the benefit of reperfusion. Experimental studies suggest that the inhibition of blood-brain barrier proteolysis reduces vasogenic oedema and the risk of haemorrhage. This recent progress in the understanding of blood-brain barrier disruption during ischaemia brings forward new therapeutic strategies using agents capable of interfering with the ischaemic cascade in order to increase the therapeutic window between the onset of ischaemia and thrombolytic reperfusion. (C) 2003 Editions scientifiques et medicales Elsevier SAS. Tous droits reserves.