SRμCT Reveals 3D Microstructural Alterations of the Vascular and Neuronal Network in a Rat Model of Chronic Compressive Thoracic Spinal Cord Injury
SRμCT Reveals 3D Microstructural Alterations of the Vascular and Neuronal Network in a Rat Model of Chronic Compressive Thoracic Spinal Cord Injury
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DOI：
10.14336/ad.2019.0529
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发表时间：
2020-06-01
影响因子：
7.4
通讯作者：
Hu, Jianzhong
中科院分区：
文献类型：
--
作者：
Jiang, Liyuan;Cao, Yong;Hu, Jianzhong
慢性胸脊髓压迫的复杂病理涉及血管和神经结构的修复过程，这在很大程度上仍然是未知的。在本研究中，我们使用同步辐射微断层扫描（SR mu CT）定量表征慢性胸脊髓压迫后血管和神经网络的三维时空变化，以进一步了解该疾病的发病机制并阐明其潜在机制。成功重建了脊髓微血管和胸脊髓神经微观结构的直接三维表征。慢性压迫后，SR mu CT显示胸脊髓血管明显减少，神经元变性，与免疫荧光染色检测的变化一致。三维形态学测量显示，压迫1个月后，胸脊髓神经血管参数明显降低，压迫未解除6个月后，情况更糟。此外，慢性压迫后明显的三维形态扭曲和中央沟动脉分支减少生动地表明，这些可能是导致胸脊髓血流量减少和神经功能缺损的潜在触发因素。我们的研究结果提出了一种新的方法，用于对慢性脊髓压迫中的神经血管修复进行定性和定量的三维分析。结果表明，压迫同时引起血管功能障碍和神经网络损伤，应被认为是慢性胸脊髓损伤后并发事件。神经保护与血管保护相结合可能为慢性胸脊髓压迫提供有前景的治疗靶点。
The complex pathology of chronic thoracic spinal cord compression involves vascular and neuroarchitectural repair processes that are still largely unknown. In this study, we used synchrotron radiation microtomography (SR mu CT) to quantitatively characterize the 3D temporal-spatial changes in the vascular and neuronal network after chronic thoracic spinal cord compression in order to obtain further insights into the pathogenesis of this disease and to elucidate its underlying mechanisms. Direct 3D characterization of the spinal cord microvasculature and neural microstructure of the thoracic spinal cord was successfully reconstructed. The significant reduction in vasculature and degeneration of neurons in the thoracic spinal cord visualized via SR mu CT after chronic compression were consistent with the changes detected by immunofluorescence staining. The 3D morphological measurements revealed significant reductions of neurovascular parameters in the thoracic spinal cord after 1 month of compression and became even worse after 6 months without relief of compression. In addition, the distinct 3D morphological twist and the decrease in branches of the central sulcal artery after chronic compression vividly displayed that these could be the potential triggers leading to blood flow reduction and neural deficits of the thoracic spinal cord. Our findings propose a novel methodology for the 3D analysis of neurovascular repair in chronic spinal cord compression, both qualitatively and quantitatively. The results indicated that compression simultaneously caused vascular dysfunction and neuronal network impairment, which should be acknowledged as concurrent events after chronic thoracic spinal cord injury. Combining neuroprotection with vasoprotection may provide promising therapeutic targets for chronic thoracic spinal cord compression.