Title
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Role of oxidative stress, angiogenesis and chemo-attractant cytokines in the pathogenesis of ischaemic protection induced by remote ischaemic conditioning : study of a human model of ischaemia-reperfusion induced vascular injury
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Author
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Abstract
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Aims We explored the effect of remote ischaemic conditioning (RIC) on endothelial function and on circulating mediators. Methods and results In 20 healthy male volunteers (mean age 31 ± 10 years), flow-mediated dilation (FMD) was measured before and after 20 min of arm ischaemia, followed by reperfusion. Remote ischaemic conditioning (RIC) was performed by applying 3 cycles of 5 min of ischaemia of the leg at the onset of index arm ischaemia. Each volunteer underwent the IR-induced vascular injury protocol with and without RIC in a crossover study design. In the control group, IR significantly reduced FMD (5.9 ± 2.9% before IR vs. 2.2 ± 3.7% after IR; p < 0.001). This effect was significantly attenuated by performing RIC (FMD of 5.5 ± 3.1% before IR vs. 4.0 ± 3.4% % after IR; p for interaction = 0.01). Serum levels of SOD and ADMA increased significantly whereas MCP-1 and VEGF levels decreased significantly. Only changes in SOD levels were significantly related to the degree of RIC induced protection (r² = 0.34; p = 0.018). Conclusion RIC has protective effects against endothelial IR injury. Our biomarker study suggests that anti-oxidative stress mediators, such as SOD, seem to be more involved in the pathogenesis of RIC-induced protection in humans than angiogenesis factors or chemo-attractant cytokines. |
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Language
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English
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Source (journal)
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Pathophysiology: the official journal of the International Society for Pathophysiology. - Amsterdam
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Publication
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Amsterdam
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2019
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ISSN
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0928-4680
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DOI
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10.1016/J.PATHOPHYS.2018.11.001
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Volume/pages
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26
:1
(2019)
, p. 53-59
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Full text (Publisher's DOI)
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Full text (open access)
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Full text (publisher's version - intranet only)
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