Transient limb ischemia induces remote preconditioning and remote postconditioning in humans by a K(ATP)-channel dependent mechanism

Transient limb ischemia administered before a prolonged ischemic insult has systemic protective effects against ischemia-reperfusion (IR) injury (remote ischemic preconditioning [RIPC]). It has been demonstrated that protection from IR can be achieved by brief periods of ischemia applied at a remote...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2007-09, Vol.116 (12), p.1386-1395
Main Authors: Loukogeorgakis, Stavros P, Williams, Rupert, Panagiotidou, Anna T, Kolvekar, Shyamsunder K, Donald, Ann, Cole, Tim J, Yellon, Derek M, Deanfield, John E, MacAllister, Raymond J
Format: Article
Language:English
Subjects:
Adult
Aged
Atherosclerosis - physiopathology
Brachial Artery - physiopathology
Endothelium, Vascular - drug effects
Endothelium, Vascular - physiopathology
Female
Forearm - blood supply
Glyburide - pharmacology
Hemorheology - drug effects
Humans
Hyperemia - physiopathology
Ischemia - physiopathology
Ischemia - therapy
Ischemic Preconditioning - methods
Leg - blood supply
Male
Middle Aged
Organ Specificity
Potassium Channel Blockers - pharmacology
Potassium Channels - drug effects
Potassium Channels - physiology
Receptors, Drug - drug effects
Receptors, Drug - physiology
Reperfusion Injury - physiopathology
Reperfusion Injury - prevention & control
Time Factors
Vasodilation - drug effects
Vasodilation - physiology
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Summary:Transient limb ischemia administered before a prolonged ischemic insult has systemic protective effects against ischemia-reperfusion (IR) injury (remote ischemic preconditioning [RIPC]). It has been demonstrated that protection from IR can be achieved by brief periods of ischemia applied at a remote site during an injurious ischemic event (remote postconditioning [RPostC]). Using an in vivo model of endothelial IR injury, we sought to determine whether RPostC occurred in humans and whether it shared mechanistic similarities with RIPC. Endothelial function was assessed by flow-mediated dilation before and after IR (20 minutes of arm ischemia followed by reperfusion). RIPC was induced by conditioning cycles of 5 minutes of ischemia and reperfusion on the contralateral arm or leg before IR. For RPostC induction, conditioning cycles were administered during the ischemic phase of IR. Oral glibenclamide was used to determine the dependence of RIPC and RPostC on K(ATP) channels. IR caused a significant reduction in flow-mediated dilation in healthy volunteers (baseline, 9.3+/-1.2% versus post-IR, 3.3+/-0.7%; P
ISSN:1524-4539
DOI:10.1161/CIRCULATIONAHA.106.653782