Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo
Acute changes in neurovascular reactivity after subarachnoid hemorrhage in vivo
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DOI：
10.1177/0271678x15621253
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发表时间：
2017-01-01
影响因子：
6.3
通讯作者：
Plesnila, Nikolaus
中科院分区：
文献类型：
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作者：
Balbi, Matilde;Koide, Masayo;Plesnila, Nikolaus
蛛网膜下腔出血引起软脑膜小动脉急性和长期的收缩。这些血管是否正常扩张神经元活动是非常感兴趣的，因为葡萄糖和氧气的输送和消耗之间的不匹配可能导致额外的神经元损伤。因此，我们研究了实验性蛛网膜下腔出血后软脑膜和实质小动脉的神经血管反应性。通过细丝穿孔或假手术使C57 BL/6小鼠经受蛛网膜下腔出血。3小时后通过前爪刺激或吸入10%CO2评估神经血管反应性。采用双光子显微镜测量脑小动脉直径。使用双光子和红外差分干涉对比显微镜测量脑切片中的神经血管耦合和星形胶质细胞尾足Ca 2+。假手术小鼠的血管扩张正常CO2和前爪刺激。蛛网膜下腔出血后3小时，软脑膜和实质小动脉的CO2反应性完全丧失，而神经血管耦合不受影响。脑切片研究也显示正常的神经血管耦合和星形胶质细胞终足Ca 2+急性蛛网膜下腔出血后的正常增加。这些研究结果表明，神经元，星形胶质细胞和实质小动脉之间的通信不受影响，在蛛网膜下腔出血后的最初几个小时，而CO2反应，这是依赖于NO信号，是完全失去。
Subarachnoid hemorrhage causes acute and long-lasting constrictions of pial arterioles. Whether these vessels dilate normally to neuronal activity is of great interest since a mismatch between delivery and consumption of glucose and oxygen may cause additional neuronal damage. Therefore, we investigated neurovascular reactivity of pial and parenchymal arterioles after experimental subarachnoid hemorrhage. C57BL/6 mice were subjected to subarachnoid hemorrhage by filament perforation or sham surgery. Neurovascular reactivity was assessed 3 h later by forepaw stimulation or inhalation of 10% CO2. Diameters of cerebral arterioles were assessed using two-photon microscopy. Neurovascular coupling and astrocytic endfoot Ca2+ were measured in brain slices using two-photon and infrared-differential interference contrast microscopy. Vessels of sham-operated mice dilated normally to CO2 and forepaw stimulation. Three hours after subarachnoid hemorrhage, CO2 reactivity was completely lost in both pial and parenchymal arterioles, while neurovascular coupling was not affected. Brain slices studies also showed normal neurovascular coupling and a normal increase in astrocytic endfoot Ca2+ acutely after subarachnoid hemorrhage. These findings suggest that communication between neurons, astrocytes, and parenchymal arterioles is not affected in the first few hours after subarachnoid hemorrhage, while CO2 reactivity, which is dependent on NO signaling, is completely lost.