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Vascular-cognitive impairment after chronic high-thoracic spinal cord injury Jia, Mengyao


Individuals living with chronic spinal cord injury (SCI) often exhibit impairments in cognitive function, which impedes their rehabilitation and possible transition into community. While 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 3rd 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 middle cerebral artery (MCA). We show that in MCA of rats with SCI, there is 55% 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 (TRPV4) channels. Compared to controls, MCAs in rats with SCI were found to have 50% more collagen I in the media of vascular wall and 37% less distensibility at physiological intralumenal pressure. Furthermore in SCI group, the cerebral blood flow (CBF) in the hippocampus was reduced by 32% in association with impairment in 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 alteration and endothelial dysfunction in cerebral arteries that likely contributes to significantly reduced CBF and vascular cognitive impairment.

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