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Cutaneous microvascular perfusion responses to insulin iontophoresis are differentially affected by insulin resistance after spinal cord injury

New Findings What is the central question of this study? What impact does insulin resistance have on cutaneous perfusion responses to insulin iontophoresis in vascular beds with markedly reduced or functionally ablated sympathetic nervous system vasomotor function resulting from spinal cord injury?...

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Bibliographic Details
Published in:Experimental physiology 2017-09, Vol.102 (9), p.1234-1244
Main Authors: Fountaine, Michael F., Cirnigliaro, Christopher M., Azarelo, Frank, Hobson, Joshua C., Tascione, Oriana, Swonger, Kirsten N., Dyson‐Hudson, Trevor, Bauman, William A.
Format: Article
Language:English
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Summary:New Findings What is the central question of this study? What impact does insulin resistance have on cutaneous perfusion responses to insulin iontophoresis in vascular beds with markedly reduced or functionally ablated sympathetic nervous system vasomotor function resulting from spinal cord injury? What is the main finding and its importance? Persons with spinal cord injury have sublesional microvascular endothelial dysfunction, as indicated by a blunted cutaneous perfusion response to acetylcholine iontophoresis, and the presence of insulin resistance has a further confounding effect on endothelium‐mediated changes to cutaneous perfusion in the lower extremities. Endothelium‐mediated mechanisms that regulate skin blood flow might play an integral role in optimizing skin perfusion in vascular beds with sympathetic nervous system vasomotor impairment, such as in spinal cord injury (SCI). Insulin is a vasoactive hormone and second messenger of nitric oxide that facilitates endothelium‐mediated dilatation. The effects of insulin resistance (IR) on sublesional cutaneous perfusion responses to insulin provocation have yet to be described in persons with SCI. Persons with SCI and an able‐bodied (AB) cohort were divided into subgroups based upon fasting plasma insulin concentration cut‐offs for IR (≥13.13 mIU ml−1) or insulin sensitivity (IS;
ISSN:0958-0670
1469-445X
DOI:10.1113/EP086239