Gasche Y, Copin J-C
Division des soins intensifs de chirurgie, département de pharmacologie, d'anesthésiologie et des soins intensifs de chirurgie, Genève, Suisse.
Ann Fr Anesth Reanim. 2003 Apr;22(4):312-9. doi: 10.1016/s0750-7658(03)00069-8.
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.
脑水肿是脑梗死的一种潜在致命并发症。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。它还引发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包括内皮细胞活化和基质金属蛋白酶对内皮基底膜的降解。组织纤溶酶原激活剂进行再灌注是改善卒中预后的唯一治疗方法。这种治疗也会增加血管源性水肿和症状性出血性转化的风险，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。对缺血期间血脑屏障破坏的这一最新认识进展提出了新的治疗策略，即使用能够干扰缺血级联反应的药物，以增加缺血发作与溶栓再灌注之间的治疗窗。
