Ken Dewitte1, Marc Claeys2, Emeline Van Craenenbroeck3, Koen Monsieurs4, Hein Heidbuchel5, Vicky Hoymans6, Tibor Stoop7. 1. Antwerp University Hospital, Emergency Department, Belgium. Electronic address: kendewitte@gmail.com. 2. Antwerp University Hospital, Department of Cardiology, Belgium. Electronic address: marc.claeys@uza.be. 3. Antwerp University Hospital, Department of Cardiology, Belgium. Electronic address: Emeline.vancraenenbroeck@uza.be. 4. Antwerp University Hospital, Emergency Department, Belgium. Electronic address: koen.monsieurs@uza.be. 5. Antwerp University Hospital, Department of Cardiology, Belgium. Electronic address: hein.heidbuchel@uza.be. 6. Laboratory for Cellular and Molecular Cardiology, Research Group Cardiovascular Diseases, Department of Translational Pathophysiological Research, University of Antwerp, Antwerp, Belgium. Electronic address: Vicky.hoymans@uza.be. 7. Antwerp University Hospital, Department of Cardiology, Belgium. Electronic address: tibor.stoop@uza.be.
Abstract
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.
RCT Entities:
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.
Authors: Petra Lujza Szabó; Christopher Dostal; Patrick Michael Pilz; Ouafa Hamza; Eylem Acar; Simon Watzinger; Shalett Mathew; Gerd Kager; Seth Hallström; Bruno K Podesser; Attila Kiss Journal: J Cardiovasc Pharmacol Ther Date: 2021-08-03 Impact factor: 2.457