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Cerebrovascular Endothelial Function is Impaired after Experimental Spinal Cord Injury
Author(s) -
Jia Mengyao,
Phillips Aaron A.,
Yung Andrew,
Kozlowski Piotr,
Krassioukov Andrei V.
Publication year - 2016
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.30.1_supplement.998.2
Subject(s) - hypercapnia , brainstem , spinal cord injury , cerebral blood flow , medicine , anesthesia , spinal cord , traumatic brain injury , neuroscience , psychology , acidosis , psychiatry
Individuals suffering from spinal cord injury (SCI) exhibit 3–4 fold increased risk of stroke and diverse cognitive deficits. Endothelial dysfunction is the first step in the malicious progression of cardiovascular diseases. In vivo measurement of endothelial health has only been performed in non‐SCI populations. The present study aims to investigate the alteration of endothelial function following high‐thoracic SCI and its association with cognitive deficits. Male Wistar rats were assigned into either the T2 complete spinal cord transected (T2‐SCI; n=7) group or sham‐injured group (SHAM; n=5). A carbogen challenge (i.e., 30% carbon dioxide) was generated to induce hypercapnia. Using arterial spin labelling, MRI was performed in both groups using a 7 Tesla scanner to measure the baseline cerebral blood flow (CBF) in brainstem and pretectal regions, as well as the alteration in cortical CBF during hypercapnia. Short‐term memory was evaluated with the Novel Object Recognition test. Cortical cerebrovascular reactivity to carbon dioxide was essentially absent in T2‐SCI, and was 85% reduced compared to Sham ( p =0.010, Figure 1). Furthermore, resting (i.e., pre‐carbogen) cerebral blood flow was reduced 44% in the brainstem ( p =0.006, Figure 1) and 30% in the pretectal area in T2‐SCI ( p =0.008, Figure 1). Recognition memory was also impaired in T2‐SCI as indicated by 19% less time spent in the novel object zone (p=0.007, Figure 2). Our study demonstratesfor the first time that in vivo endothelial function (i.e., reactivity to carbon dioxide) in cerebrovasculature is impaired following high‐thoracic SCI and is associated with vascular‐cognitive decline. This study identified a potential therapeutic target for reducing stroke risk and improving cognitive function after SCI. Support or Funding Information AAP: Craig H. Neilsen Foundation Postdoctoral Fellowship 337427, Heart and Stroke Foundation of Canada Research Fellowship, Michael Smith Foundation for Health Research Postdoctoral Fellowship AVK: Canadian Institute of Health Research, Craig H. Neilsen Foundation. 1 Regional cerebral blood flow(CBF) before and during hypercapniaA , Alteration in cortical CBF during hypercapnia is significantly reduced in T2‐SCI animals. B , Resting CBF is also reduced in the brain stem and pretectal areas after SCI. * indicates significantly difference ( p <0.05).2 Short‐term memory assessment by Novel Object Recognition TestT2‐SCI animals spent significantly less time in the novel object zone (i.e. impaired short‐term memory). * indicates significantly difference ( p <0.05).