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Vascular-Cognitive Impairment following High-Thoracic Spinal Cord Injury Is Associated with Structural and Functional Maladaptations in Cerebrovasculature.
Journal of Neurotrauma ( IF 4.2 ) Pub Date : 2020-08-27 , DOI: 10.1089/neu.2019.6913
Rahul Sachdeva 1, 2 , Mengyao Jia 1, 2 , Shaoxun Wang 3 , Andrew Yung 1, 2 , Mei Mu Zi Zheng 1, 2 , Amanda H X Lee 1, 2 , Aaron Monga 1, 2 , Sarah Leong 2 , Piotr Kozlowski 1, 2 , Fan Fan 3 , Richard J Roman 3 , Aaron A Phillips 4 , Andrei V Krassioukov 1, 2, 5
Affiliation  

Individuals living with chronic spinal cord injury (SCI) often exhibit impairments in cognitive function, which impede their rehabilitation and transition into the community. Although a number of clinical studies have demonstrated the impact of impaired cardiovascular control on cognitive impairment, the mechanistic understanding of this deleterious relationship is still lacking. The present study investigates whether chronic disruption of cardiovascular control following experimental SCI results in cerebrovascular decline and vascular cognitive impairment. Fourteen weeks following a high thoracic SCI (at the third thoracic segment), rats were subjected to a battery of in vivo and in vitro physiological assessments, cognitive-behavioral tests, and immunohistochemical approaches to investigate changes in cerebrovascular structure and function in the middle cerebral artery (MCA). We show that in the MCA of rats with SCI, there is a 55% (SCI vs. control: 13.4 ± 1.9% vs. 29.63 ± 2.8%, respectively) reduction in the maximal vasodilator response to carbachol, which is associated with reduced expression of endothelial marker cluster of differentiation 31 (CD31) and transient receptor potential cation channel 4 (TRPV 4) channels. Compared with controls, MCAs in rats with SCI were found to have 50% (SCI vs. control: 1.5 ± 0.2 vs. 1 ± 0.1 a.u., respectively) more collagen 1 in the media of vascular wall and 37% (SCI vs. control: 30.5 ± 2.9% vs. 42.0 ± 4.0%, respectively) less distensibility at physiological intraluminal pressure. Further, the cerebral blood flow (CBF) in the hippocampus was reduced by 32% in the SCI group (SCI vs. control: 44.3 ± 4.5 mL/100 g/min vs. 65.0 ± 7.2 mL/100 g/min, respectively) in association with impairment of short-term memory based on a novel object recognition test. There were no changes in the sympathetic innervation of the vasculature and passive structure in the SCI group. Chronic experimental SCI is associated with structural alterations and endothelial dysfunction in cerebral arteries that likely contribute to significantly reduced CBF and vascular cognitive impairment.

中文翻译:

高胸段脊髓损伤后的血管认知障碍与脑血管系统的结构和功能性适应不良有关。

患有慢性脊髓损伤 (SCI) 的人经常表现出认知功能障碍,这阻碍了他们的康复和融入社区。尽管许多临床研究已经证明心血管控制受损对认知障碍的影响,但仍然缺乏对这种有害关系的机制理解。本研究调查实验性 SCI 后心血管控制的慢性破坏是否会导致脑血管衰退和血管认知障碍。高胸段 SCI(在第三胸段)后 14 周,大鼠接受了一系列体内体外实验生理评估、认知行为测试和免疫组织化学方法来研究大脑中动脉 (MCA) 脑血管结构和功能的变化。我们表明,在 SCI 大鼠的 MCA 中,对卡巴胆碱的最大血管舒张反应降低了 55%(SCI 与对照:13.4 ± 1.9% 与 29.63 ± 2.8%),这与表达降低有关内皮细胞分化标记簇 31 (CD31) 和瞬时受体电位阳离子通道 4 (TRPV 4) 通道。与对照组相比,发现 SCI 大鼠的 MCA 在血管壁中层中具有 50%(SCI 与对照组:1.5 ± 0.2 与 1 ± 0.1 au)更多的胶原蛋白 1 和 37%(SCI 与对照组) : 30.5 ± 2.9% 与 42.0 ± 4.0% 分别) 在生理腔内压力下的膨胀性降低。更远,SCI 组的海马脑血流量 (CBF) 减少了 32%(SCI 与对照组:分别为 44.3 ± 4.5 mL/100 g/min 和 65.0 ± 7.2 mL/100 g/min)相关联基于新的物体识别测试的短期记忆障碍。SCI 组的脉管系统和被动结构的交感神经支配没有变化。慢性实验性 SCI 与脑动脉的结构改变和内皮功能障碍有关,这可能有助于显着降低 CBF 和血管认知障碍。SCI 组的脉管系统和被动结构的交感神经支配没有变化。慢性实验性 SCI 与脑动脉的结构改变和内皮功能障碍有关,这可能有助于显着降低 CBF 和血管认知障碍。SCI 组的脉管系统和被动结构的交感神经支配没有变化。慢性实验性 SCI 与脑动脉的结构改变和内皮功能障碍有关,这可能有助于显着降低 CBF 和血管认知障碍。
更新日期:2020-09-12
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