Abstract：
Brain oedema is thought to form and to clear through the use of water-protein channels, aquaporin-4 (AQP4), which are found in the astrocyte endfeet. The model developed here is used to study the function of AQP4 in the formation and elimination of oedema fluid in ischaemia-reperfusion injury. The cerebral space is assumed to be made of four fluid compartments: astrocyte, neuron, ECS and blood microvessels, and a solid matrix for the tissue, and this is modelled using multiple-network poroelastic theory. AQP4 allows the movement of water between astrocyte and the ECS and the microvessels. It is found that the presence of AQP4 may help in reducing vasogenic oedema shown by a decrease in brain tissue extracellular pressure. However, the astrocyte pressure will increase to compensate for this decrease, which may lead to cytotoxic oedema. In addition, the swelling will also depend on the ionic concentrations in the astrocyte and extracellular space, which may change after ischaemic stroke. Understanding the role of AQP4 in oedema may thus help the development of a treatment plan in reducing brain swelling after ischaemia-reperfusion.
摘要：
脑水肿被认为是通过使用水蛋白通道形成和清除的，水通道蛋白-4(AQP4),在星形胶质细胞的终足中发现。本文建立的模型用于研究AQP4在缺血再灌注损伤中水肿液的形成和消除中的功能。假定大脑空间由四个流体隔室组成：星形胶质细胞，神经元,ECS和微血管，和组织的固体基质，这是用多网络多孔弹性理论建模的。AQP4允许水在星形胶质细胞与ECS和微血管之间移动。发现AQP4的存在可能有助于减少由脑组织细胞外压力降低所显示的血管源性水肿。然而,星形胶质细胞的压力会增加来补偿这种减少，这可能导致细胞毒性水肿。此外,肿胀还取决于星形胶质细胞和细胞外空间中的离子浓度，缺血性中风后可能会发生变化。因此，了解AQP4在水肿中的作用可能有助于制定减少缺血再灌注后脑肿胀的治疗计划。
