高血压性脑出血后脑水肿形成机制的研究进展

Research Advancement about Mechanism of Cerebral Edema After Hypertension Cerebral Hemorrhage

脑出血是脑卒中的一个类型，具有较高的发病率和病死率。脑水肿的产生是脑出血后二次损伤发生的关键性因素，血肿旁水肿的形成过程始于脑出血的早期。凝血酶在促成血肿周围水肿上的中心作用已经得到证明，凝血酶抑制剂可使水肿形成减少。红细胞、血红蛋白、铁离子、血小板、白细胞及细胞因子与脑水肿的发生有密切关系，血肿的占位损伤及继发性脑缺血对脑水肿的形成有促进作用。基质金属蛋自酶是脑出血的并发症和结构上的重要标志物。

Intracerebtal hemorrhage （ICH） is a specific subtype of stroke with high morbidity and mortality. Cerebral edema is the crucial factor of the second injury after hypertension cerebral hemorrhage. The formation of perihematoma edema begins at the early stage of ICH. Thrombin has been identified to play an important role in promoting perihematoma edema, thrombin inhibitors can reduce the edema formation. Red blood cell, hemoglobin,iron ion, platelet, leukocyte and cytokines are all related to the genesis of cerebral edema. Space-occupying lesions of hematoma and secondary ischemia around hematoma can promote the formation of cerebral edema. Matrix metalloproteinases（MMPs） are important markers of the complications and structure of ICH.