ArticleJournal of neurobiology and physiology2020
Duration and magnitude of bidirectional fluctuation in blood pressure: the link between cerebrovascular dysfunction and cognitive impairment following spinal cord injury.
Article in Journal of neurobiology and physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 4 citations in OpenAlex.
- 20-HETE-promoted cerebral blood flow autoregulation is associated with enhanced pericyte contractility.Prostaglandins & other lipid mediators · 2021Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Individuals with spinal cord injury (SCI) have a significantly increased risk for cognitive impairment that is associated with cerebrovascular remodeling and endothelial dysfunction. The sub-acute stage following high thoracic SCI is characterized by increased fibrosis and stiffness of cerebral arteries. However, a more prolonged duration after SCI exacerbates cerebrovascular injury by damaging endothelium. Endothelial dysfunction is associated with reduced expression of transient receptor potential cation channel 4 that mediates the production of nitric oxide and epoxyeicosatrienoic acids following shear stress and the response to carbachol and other endothelium-dependent vasodilators. Reduced expression of CD31 in cerebral arteries also suggests the loss of endothelial cell integrity following chronic SCI. Repetitively transient hypertension and intermittent hypotension contribute to cerebrovascular endothelial dysfunction in the animals with a sub-acute stage of high thoracic SCI. The increase in vascular remodeling and endothelial dysfunction ultimately reduce cerebral blood flow, which promotes cerebral hypoperfusion and cognitive dysfunction in the chronic phase of SCI. In conclusion, the duration and magnitude of fluctuations in blood pressure after SCI play a vital role in the onset and progress of cerebrovascular dysfunction, which promotes the development of cognitive impairment.
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Registered trials
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