3D analysis of intracortical microvasculature during chronic hypoxia in mouse brains.
3D analysis of intracortical microvasculature during chronic hypoxia in mouse brains.
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DOI：
10.1007/978-1-4614-4989-8_50
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发表时间：
2013
影响因子：
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通讯作者：
K. Yoshihara;H. Takuwa;I. Kanno;S. Okawa;Yukio Yamada;K. Masamoto
中科院分区：
文献类型：
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作者：
K. Yoshihara;H. Takuwa;I. Kanno;S. Okawa;Yukio Yamada;K. Masamoto
本研究的目的是确定脑微血管系统在慢性缺氧时改变其网络的时间和位置。为了确定缺氧诱导的结构适应，我们纵向成像皮质微血管在同一位置内的小鼠体感皮质与双光子显微镜重复长达1个月，在连续暴露于缺氧（无论是8或10%的氧气条件）。双光子显微镜的方法使得有可能跟踪从皮质表面小动脉到小静脉的3D路径，深度为0.8 mm。然后在分支处将网络通路分成单独的血管段，并测量它们的直径和长度。在3D重建图像（0.46 × 0.46 × 0.80 mm ~ 3）中，在20-460 μm的深度范围内，观察到穿通小动脉和出射静脉之间的3-11个血管段。毛细血管（直径<7 μm）平均长度为67 ± 46 μm，不受缺氧影响。与此相反，暴露于8%和10%缺氧后1周，毛细血管直径分别增加1.4 ± 0.3和1.2 ± 0.2倍。暴露后3周，8%和10%低氧条件下毛细血管直径分别达到8.5 ± 1.9和6.7 ± 1.8 μm，分别为低氧前的1.8 ± 0.5和1.4 ± 0.3倍。与实质毛细血管相比，穿透性小动脉（1.4 ± 0.2和1.2 ± 0.2倍增加）和新生静脉（1.3 ± 0.2和1.3 ± 0.2倍增加）的血管舒张显示相对较小的直径变化。这些结果表明，脑实质毛细血管是慢性缺氧时对氧环境作出反应的主要部位。
The purpose of this study is to determine when and where the brain microvasculature changes its network in response to chronic hypoxia. To identify the hypoxia-induced structural adaptation, we longitudinally imaged cortical microvasculature at the same location within a mouse somatosensory cortex with two-photon microscopy repeatedly for up to 1 month during continuous exposure to hypoxia (either 8 or 10% oxygen conditions). The two-photon microscopy approach made it possible to track a 3D pathway from a cortical surface arteriole to a venule up to a depth of 0.8 mm from the cortical surface. The network pathway was then divided into individual vessel segments at the branches, and their diameters and lengths were measured. We observed 3–11 vessel segments between the penetrating arteriole and the emerging vein over the depths of 20–460 μm within the 3D reconstructed image (0.46 × 0.46 × 0.80 mm3). The average length of the individual capillaries (<7 μm in diameter) was 67 ± 46 μm, which was not influenced by hypoxia. In contrast, 1.4 ± 0.3 and 1.2 ± 0.2 fold increases of the capillary diameter were observed 1 week after exposure to 8 % and 10% hypoxia, respectively. At 3 weeks from the exposure, the capillary diameter reached 8.5 ± 1.9 and 6.7 ± 1.8 μm in 8% and 10 % hypoxic conditions, respectively, which accounted for the 1.8 ± 0.5 and 1.4 ± 0.3 fold increases relative to those of the prehypoxic condition. The vasodilation of penetrating arterioles (1.4 ± 0.2 and 1.2 ± 0.2 fold increases) and emerging veins (1.3 ± 0.2 and 1.3 ± 0.2 fold increases) showed relatively small diameter changes compared with the parenchymal capillaries. These findings indicate that parenchymal capillaries are the major site responding to the oxygen environment during chronic hypoxia.