Source:http://linkedlifedata.com/resource/pubmed/id/12791590
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
4
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pubmed:dateCreated |
2003-9-12
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pubmed:abstractText |
The aim of this study was to investigate the efficacy and mechanism of action of a noninvasive remote ischemic preconditioning (IPC) technique for the protection of multiple distant skeletal muscles against ischemic necrosis (infarction). It was observed in the pig that three cycles of 10-min occlusion and reperfusion in a hindlimb by tourniquet application reduced the infarction of latissimus dorsi (LD), gracilis (GC), and rectus abdominis (RA) muscle flaps by 55%, 60%, and 55%, respectively, compared with their corresponding control (n = 6, P < 0.01) when they were subsequently subjected to 4 h of ischemia and 48 h of reperfusion. This infarct-protective effect of remote IPC in LD muscle flaps was abolished by an intravenous bolus injection of the nonselective opioid receptor antagonist naloxone (3 mg/kg) 10 min before remote IPC and a continuous intravenous infusion (3 mg/kg) during remote IPC and by an intravenous bolus injection of the selective delta 1-opioid receptor antagonist 7-benzylidenealtrexone maleate (3 mg/kg). However, this infarct-protective effect of remote IPC was not affected by an intravenous bolus injection of the ganglionic blocker hexamethonium chloride (20 mg/kg) or the nonspecific adenosine receptor antagonist 8-(p-sulfophenyl)theophylline (10 mg/kg) or by a local intra-arterial injection of the adenosine1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (3 mg/muscle flap) given 10 min before remote IPC. It was also observed that this remote IPC of skeletal muscle against infarction was associated with a slower rate of muscle ATP depletion during the 4 h of sustained ischemia and a reduced muscle neutrophilic myeloperoxidase activity after 1.5 h of reperfusion. These observations led us to speculate that noninvasive remote IPC by brief cycles of occlusion and reperfusion in a pig hindlimb is effective in global protection of skeletal muscle against infarction. This infarct-protective effect is most likely triggered by the activation of opioid receptors in the skeletal muscle, and remote IPC is associated with an energy-sparing effect during sustained ischemia and attenuation of neutrophil accumulation during reperfusion.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Adenosine Triphosphate,
http://linkedlifedata.com/resource/pubmed/chemical/Ganglionic Blockers,
http://linkedlifedata.com/resource/pubmed/chemical/Hexamethonium,
http://linkedlifedata.com/resource/pubmed/chemical/Lactic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Opioid
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
0363-6135
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
285
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
H1435-43
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12791590-Abdomen,
pubmed-meshheading:12791590-Adenosine Triphosphate,
pubmed-meshheading:12791590-Animals,
pubmed-meshheading:12791590-Ganglionic Blockers,
pubmed-meshheading:12791590-Hexamethonium,
pubmed-meshheading:12791590-Hindlimb,
pubmed-meshheading:12791590-Infarction,
pubmed-meshheading:12791590-Ischemic Preconditioning,
pubmed-meshheading:12791590-Lactic Acid,
pubmed-meshheading:12791590-Male,
pubmed-meshheading:12791590-Muscle, Skeletal,
pubmed-meshheading:12791590-Neutrophils,
pubmed-meshheading:12791590-Peroxidase,
pubmed-meshheading:12791590-Receptors, Opioid,
pubmed-meshheading:12791590-Reperfusion Injury,
pubmed-meshheading:12791590-Surgical Flaps,
pubmed-meshheading:12791590-Swine,
pubmed-meshheading:12791590-Thigh,
pubmed-meshheading:12791590-Thorax
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pubmed:year |
2003
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pubmed:articleTitle |
Noninvasive remote ischemic preconditioning for global protection of skeletal muscle against infarction.
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pubmed:affiliation |
Research Institute, The Hospital for Sick Children, and Department of Surgery, University of Toronto, Ontario, Canada M5G 1X8.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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