The aquaporin-4 (AQP4) pool in the perivascular astrocyte membranes has been shown to be critically involved in the formation and dissolution of brain edema. Cerebral edema is a major cause of morbidity and mortality in stroke. It is therefore essential to know whether the perivascular pool of AQP4 is up- or down-regulated after an ischemic insult, because such changes would determine the time course of edema formation. Here we demonstrate by quantitative immunogold cytochemistry that the ischemic striatum and neocortex show distinct patterns of AQP4 expression in the reperfusion phase after 90 min of middle cerebral artery occlusion. The striatal core displays a loss of perivascular AQP4 at 24 hr of reperfusion with no sign of subsequent recovery. The most affected part of the cortex also exhibits loss of perivascular AQP4. This loss is of magnitude similar to that of the striatal core, but it shows a partial recovery toward 72 hr of reperfusion. By freeze fracture we show that the loss of perivascular AQP4 is associated with the disappearance of the square lattices of particles that normally are distinct features of the perivascular astrocyte membrane. The cortical border zone differs from the central part of the ischemic lesion by showing no loss of perivascular AQP4 at 24 hr of reperfusion but rather a slight increase. These data indicate that the size of the AQP4 pool that controls the exchange of fluid between brain and blood during edema formation and dissolution is subject to large and region-specific changes in the reperfusion phase.

译文

:血管周星形胶质细胞膜中的aquaporin-4(AQP4)池已被证明与脑水肿的形成和消解密切相关。脑水肿是中风发病和死亡的主要原因。因此,至关重要的是要知道缺血性损伤后AQP4的血管周池是上调还是下调,因为这种变化将决定水肿形成的时间过程。在这里,我们通过定量免疫金细胞化学证明,缺血性纹状体和新皮层在大脑中动脉闭塞90分钟后的再灌注阶段显示出不同的AQP4表达模式。纹状体核心在再灌注24小时时显示血管周围AQP4丧失,没有随后恢复的迹象。皮层最受影响的部分还表现出血管周AQP4的丢失。这种损失的程度与纹状体核心的损失相似,但是显示出在再灌注72小时后部分恢复。通过冷冻断裂,我们显示血管周围AQP4的丧失与正常情况下是血管周星形胶质细胞膜独特特征的颗粒方格消失有关。皮质边界区与缺血性病变的中心部分不同,在再灌注24小时时血管周围AQP4并未丢失,但略有增加。这些数据表明,在水肿形成和溶解过程中,控制大脑和血液之间的流体交换的AQP4库的大小在再灌注阶段会受到较大的区域特定变化的影响。

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