Xu Miao, Su Wei, Xu Qiu-ping
Department of Critical Care Medicine, Sir Run Run Shaw Hospital, Medical College of Zhejiang University and Sir Run Run Shaw Institute of Clinical Medicine, Hangzhou, China.
Chin J Traumatol. 2010 Apr 1;13(2):103-10.
Brain edema leading to an expansion of brain volume has a crucial impact on morbidity and mortality following traumatic brain injury as it increases intracranial pressure, impairs cerebral perfusion and oxygenation, and contributes to additional ischemic injuries. Classically, two major types of traumatic brain edema exist: "vasogenic" and "cytotoxic/cellular". However, the cellular and molecular mechanisms contributing to the development/resolution of traumatic brain edema are poorly understood and no effective drugs can be used now. Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 has been proposed as a novel drug target in brain edema. These findings suggest that modulation of AQP4 expression or function may be beneficial in traumatic brain edema.
脑损伤后，脑水肿导致脑容量增加，对发病率和死亡率有着至关重要的影响，因为它会升高颅内压，损害脑灌注和氧合，并导致额外的缺血性损伤。传统上，创伤性脑水肿主要存在两种类型：“血管源性”和“细胞毒性/细胞性”。然而，导致创伤性脑水肿发生/消退的细胞和分子机制仍知之甚少，目前尚无有效的药物可用。水通道蛋白4（AQP4）是一种在脑中大量表达的水通道蛋白，主要存在于脑实质与主要液体腔隙（包括脑脊液和血液）之间边界处的星形胶质细胞足突中。这种分布表明AQP4控制着水进出脑实质的通量。在细胞毒性水肿中，AQP4缺失会减缓水进入脑的速度，而在血管源性水肿中，AQP4缺失会降低水从脑实质流出的速度。AQP4已被提议作为脑水肿的新型药物靶点。这些发现表明，调节AQP4的表达或功能可能对创伤性脑水肿有益。
