Postconditioning protects against endothelial ischemia-reperfusion injury in the human forearm

Hypoxic cell death follows interruption of blood supply to tissues. Although successful restoration of blood flow is mandatory for salvage of ischemic tissues, reperfusion can paradoxically place tissues at risk of further injury. Brief periods of ischemia applied at the onset of reperfusion have be...

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Bibliographic Details
Published in:Circulation (New York, N.Y.) N.Y.), 2006-02, Vol.113 (7), p.1015-1019
Main Authors: LOUKOGEORGAKIS, Stavros P, PANAGIOTIDOU, Anna T, YELLON, Derek M, DEANFIELD, John E, MACALLISTER, Raymond J
Format: Article
Language:English
Subjects:
Adolescent
Adult
Antihypertensive agents
Biological and medical sciences
Blood and lymphatic vessels
Brachial Artery - physiopathology
Cardiology. Vascular system
Cardiovascular system
Diseases of the peripheral vessels. Diseases of the vena cava. Miscellaneous
Endothelium, Vascular - pathology
Endothelium, Vascular - physiopathology
Female
Forearm - blood supply
Humans
Ischemic Preconditioning - methods
Male
Medical sciences
Pharmacology. Drug treatments
Reperfusion - methods
Reperfusion Injury - prevention & control
Time Factors
Treatment Outcome
Vasodilation
Vasodilator agents. Cerebral vasodilators
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Summary:Hypoxic cell death follows interruption of blood supply to tissues. Although successful restoration of blood flow is mandatory for salvage of ischemic tissues, reperfusion can paradoxically place tissues at risk of further injury. Brief periods of ischemia applied at the onset of reperfusion have been shown to reduce ischemia-reperfusion (IR) injury, a phenomenon called postconditioning. The aim of this study was to determine whether postconditioning protects against endothelial IR injury in humans, in vivo. Brachial artery endothelial function was assessed by vascular ultrasound to measure flow-mediated dilation (FMD) in response to forearm reactive hyperemia. FMD was measured before and after IR (20 minutes of arm ischemia followed by 20 minutes of reperfusion) in healthy volunteers. To test the protective effects of postconditioning, 3 cycles of reperfusion followed by ischemia (each lasting 10 or 30 seconds) were applied immediately after 20 minutes of arm ischemia. To determine whether postconditioning needs to be applied at the onset of reperfusion, a 1-minute period of arm reperfusion was allowed before the application of the 10-second postconditioning stimulus. IR caused endothelial dysfunction (FMD 9.1+/-1.2% pre-IR, 3.6+/-0.7% post-IR, P
ISSN:0009-7322
1524-4539
DOI:10.1161/circulationaha.105.590398