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Publication year
2006Source
Journal of the American College of Cardiology, 48, 4, (2006), pp. 700-7ISSN
Publication type
Article / Letter to editor
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Organization
Pharmacology-Toxicology
Nuclear Medicine
Cardio Thoracic Surgery
Former Organization
Pharmacology/Toxicology
Thoracic Cardiac Surgery
Journal title
Journal of the American College of Cardiology
Volume
vol. 48
Issue
iss. 4
Page start
p. 700
Page end
p. 7
Subject
N4i 1: Pathogenesis and modulation of inflammation; NCEBP 14: Cardiovascular diseases; NCMLS 2: Immune Regulation; ONCOL 3: Translational research; ONCOL 5: Aetiology, screening and detection; UMCN 2.1: Heart, lung and circulation; UMCN 2.2: Vascular medicine and diabetesAbstract
OBJECTIVES: We studied whether caffeine impairs protection by ischemic preconditioning (IP) in humans. BACKGROUND: Ischemic preconditioning is critically dependent on adenosine receptor stimulation. We hypothesize that the adenosine receptor antagonist caffeine blocks the protective effect of IP. METHODS: In vivo ischemia-reperfusion injury was assessed in the thenar muscle by 99mTc-annexin A5 scintigraphy. Forty-two healthy volunteers performed forearm ischemic exercise. In 24 subjects, this was preceded by a stimulus for IP. In a randomized double-blinded design, the subjects received caffeine (4 mg/kg) or saline intravenously before the experiment. At reperfusion, 99mTc-annexin A5 was administered intravenously. Targeting of annexin was quantified by region-of-interest analysis, and expressed as percentage difference between experimental and contralateral hand. In vitro, we assessed recovery of contractile function of human atrial trabeculae, harvested during heart surgery, as functional end point of ischemia-reperfusion injury. Field-stimulated contraction was quantified at baseline and after simulated ischemia-reperfusion, in a paired approach with and without 5 min of IP, in the presence (n=13) or absence (n = 17) of caffeine (10 mg/l). RESULTS: Ischemic preconditioning reduced annexin targeting in the absence of caffeine (from 13 +/- 3% to 7 +/- 1% at 1 h, and from 19 +/- 2% to 9 +/- 3% at 4 h after reperfusion, p = 0.006), but not after caffeine administration (targeting 11 +/- 2% and 16 +/- 3% at 1 and 4 h). In vitro, IP improved post-ischemic functional recovery in the control group, but not in the caffeine group (8 +/- 3% vs. -8 +/- 5%, p=0.003). CONCLUSIONS: Caffeine abolishes IP in 2 human models at a dose equivalent to the drinking of 2 to 4 cups of coffee. (The Effect of Caffeine on Ischemic Preconditioning; http://clinicaltrials.gov/ct/show/NCT00184912?order=1; NCT00184912).
This item appears in the following Collection(s)
- Academic publications [238441]
- Electronic publications [122508]
- Faculty of Medical Sciences [90373]
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