Remote ischemic conditioning protects against endothelial ischemia-reperfusion injury via a glucagon-like peptide-1 receptor-mediated mechanism in humans.
Adult
Brachial Artery
/ physiopathology
Endothelium, Vascular
/ metabolism
Glucagon-Like Peptide-1 Receptor
/ antagonists & inhibitors
Healthy Volunteers
Humans
Injections, Intravenous
Ischemic Preconditioning, Myocardial
/ methods
Male
Myocardial Reperfusion Injury
/ metabolism
Peptide Fragments
/ administration & dosage
Vasodilation
/ physiology
Cardioprotection
Endothelial function
Flow-mediated dilatation
Glucagon-like peptide-1
Ischemia-reperfusion
Remote ischemic conditioning
Journal
International journal of cardiology
ISSN: 1874-1754
Titre abrégé: Int J Cardiol
Pays: Netherlands
ID NLM: 8200291
Informations de publication
Date de publication:
01 Jan 2019
01 Jan 2019
Historique:
received:
08
05
2018
revised:
03
09
2018
accepted:
17
09
2018
pubmed:
1
10
2018
medline:
23
7
2019
entrez:
1
10
2018
Statut:
ppublish
Résumé
Remote ischemic conditioning (RIC), i.e. short cycles of ischemia and reperfusion in remote tissue, is a novel approach to protect against myocardial ischemia-reperfusion injury in ST-elevation myocardial infarction. The nature of the factors transmitting the protective effect of RIC remains unknown, and both neuronal and hormonal mechanisms appear to be involved. A recent study indicated involvement of glucagon-like peptide-1 (GLP-1) regulated by the vagal nerve in RIC in rats. In the present study we aimed to investigate whether the protective effect of RIC is mediated by a GLP-1 receptor-dependent mechanism in humans. Endothelial function was determined from flow-mediated dilatation (FMD) of the brachial artery before and after 20 min of forearm ischemia and 20 min of reperfusion in twelve healthy subjects on three occasions: (A) ischemia-reperfusion without intervention, (B) ischemia-reperfusion + RIC and (C) iv administration of the GLP-1 receptor antagonist exendin(9-39) + ischemia-reperfusion + RIC. Ischemia-reperfusion reduced FMD from 4.7 ± 0.8% at baseline to 1.5 ± 0.4% (p < 0.01). RIC protected from the impairment in FMD induced by ischemia-reperfusion (4.6 ± 1.1% at baseline vs. 5.0 ± 1.1% following ischemia-reperfusion). Exendin(9-39) abolished the protection induced by RIC (FMD 4.9 ± 0.9% at baseline vs. 1.4 ± 1.3% following ischemia-reperfusion; p < 0.01) but did not affect basal FMD. Plasma GLP-1 levels did not change significantly between examinations. The present study is the first to suggest that RIC protects against endothelial ischemia-reperfusion injury via a GLP-1 receptor-mediated mechanism in humans.
Sections du résumé
BACKGROUND
BACKGROUND
Remote ischemic conditioning (RIC), i.e. short cycles of ischemia and reperfusion in remote tissue, is a novel approach to protect against myocardial ischemia-reperfusion injury in ST-elevation myocardial infarction. The nature of the factors transmitting the protective effect of RIC remains unknown, and both neuronal and hormonal mechanisms appear to be involved. A recent study indicated involvement of glucagon-like peptide-1 (GLP-1) regulated by the vagal nerve in RIC in rats. In the present study we aimed to investigate whether the protective effect of RIC is mediated by a GLP-1 receptor-dependent mechanism in humans.
METHODS
METHODS
Endothelial function was determined from flow-mediated dilatation (FMD) of the brachial artery before and after 20 min of forearm ischemia and 20 min of reperfusion in twelve healthy subjects on three occasions: (A) ischemia-reperfusion without intervention, (B) ischemia-reperfusion + RIC and (C) iv administration of the GLP-1 receptor antagonist exendin(9-39) + ischemia-reperfusion + RIC.
RESULTS
RESULTS
Ischemia-reperfusion reduced FMD from 4.7 ± 0.8% at baseline to 1.5 ± 0.4% (p < 0.01). RIC protected from the impairment in FMD induced by ischemia-reperfusion (4.6 ± 1.1% at baseline vs. 5.0 ± 1.1% following ischemia-reperfusion). Exendin(9-39) abolished the protection induced by RIC (FMD 4.9 ± 0.9% at baseline vs. 1.4 ± 1.3% following ischemia-reperfusion; p < 0.01) but did not affect basal FMD. Plasma GLP-1 levels did not change significantly between examinations.
CONCLUSION
CONCLUSIONS
The present study is the first to suggest that RIC protects against endothelial ischemia-reperfusion injury via a GLP-1 receptor-mediated mechanism in humans.
Identifiants
pubmed: 30268384
pii: S0167-5273(18)32752-9
doi: 10.1016/j.ijcard.2018.09.061
pii:
doi:
Substances chimiques
Glucagon-Like Peptide-1 Receptor
0
Peptide Fragments
0
exendin (9-39)
5313W10MYT
Types de publication
Journal Article
Randomized Controlled Trial
Langues
eng
Sous-ensembles de citation
IM
Pagination
40-44Informations de copyright
Copyright © 2018 Elsevier B.V. All rights reserved.