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Vascular‐cognitive Impairment after Chronic Experimental High‐thoracic Spinal Cord Injury
Author(s) -
Jia Mengyao,
Sachdeva Rahul,
Wang Shaoxun,
Yung Andrew,
Zheng Mei Mu Zi,
Lee Amanda HX,
Leong Sarah,
Kozlowski Piotr,
Fan Fan,
Roman Richard J.,
Phillips Aaron A,
Krassioukov Andrei V
Publication year - 2019
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.2019.33.1_supplement.688.15
Subject(s) - medicine , spinal cord injury , cerebral blood flow , magnetic resonance imaging , blood pressure , cardiology , anesthesia , spinal cord , radiology , psychiatry
Cognitive impairment is present in 64% individuals with spinal cord injury (SCI), affecting their attention, memory, learning and studying abilities, which are essential for post‐injury rehabilitation and possible transition into community. Previous studies from our group have reported the presence of vascular‐cognitive impairment in SCI individuals. However, a direct link between SCI‐associated vascular dysfunction and cognitive deficits hasn't been established. Objective To designing a pre‐clinical model to investigate cardiovascular, cerebrovascular, and cognitive function following chronic high‐thoracic SCI. Methods Twenty‐eight male Wistar rats were assigned to uninjured group (CON, n=14) and T3‐level spinal transection group (SCI, n=14). Fourteen weeks after injury, cognitive function and cerebral blood flow from both group were evaluated using novel object recognition test and magnetic resonance imaging (MRI) respectively. Moreover, in vivo and in vitro physiological assessments, as well as histological assessment in cerebral vasculature were conducted. Results Our animal model demonstrates autonomic disreflexia (AD) event (41.860 mmHg increase in systolic blood pressure) induced by colorectal distension, clinically relevant to unstable blood pressure following SCI. We conclude that chronic high‐thoracic SCI leads to 1) short‐memory loss ( p =0.0225), 2) cerebral hypoperfusion (32% reduction in baseline cerebral blood flow, p =0.0277) and 3) cerebrovascular dysfunctions, including endothelial dysfunction associated with reduced endothelial TRPV 4 expression, and 70% increased collagen I deposition. Conclusion This study provides evidence that vascular‐cognitive impairment occurs at chronic stage of SCI and highlighting TRPV 4 as a potential therapeutic target to improve post‐injury cognitive and cerebrovascular health. Support or Funding Information Canadian Institute of Health Research, Heart and Stroke Foundation of Canada This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal .

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