| Role of Erk1/2, p70s6K, and eNOS in isoflurane-induced cardioprotection during early reperfusion in vivo. | |
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MedLine Citation:
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PMID: 16434759 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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PURPOSE: Administration of isoflurane during early reperfusion after prolonged coronary artery occlusion decreases myocardial infarct size by activating phosphatidylinositol-3-kinase (PI3K) signal transduction. The extracellular signal-related kinases (Erk1/2) represent a redundant mechanism by which signaling elements downstream from PI3K, including 70-kDA ribosomal protein s6 kinase (p70s6K) and endothelial nitric oxide synthase (eNOS), may be activated to reduce reperfusion injury. We tested the hypothesis Erk1/2, p70s6K, and eNOS mediate isoflurane-induced postconditioning in rabbit myocardium in vivo. METHODS: Barbiturate-anesthetized rabbits (n = 78) instrumented for measurement of systemic hemodynamics were subjected to a 30-min coronary occlusion followed by three hours reperfusion. Rabbits were randomly assigned to receive 0.9% saline (control), the Erk1/2 inhibitor PD 098059 (2 mg x kg(-1)), the p70s6K inhibitor rapamycin (0.25 mg x kg(-1)), the nonselective nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME; 10 mg x kg(-1)), the selective inducible NOS antagonist aminoguanidine hydrochloride (AG, 300 mg x kg(-1)), or the selective neuronal NOS inhibitor 7-nitroindazole (7-NI, 50 mg x kg(-1)) in the presence or absence of 1.0 minimum alveolar concentration isoflurane administered for three minutes before and two minutes after reperfusion. RESULTS: Brief exposure to 1.0 minimum alveolar concentration isoflurane reduced (P < 0.05) infarct size (21 +/- 4% [mean +/- SD] of left ventricle area at risk, respectively; triphenyltetrazolium staining) as compared to control (41 +/- 5%). PD 098059, rapamycin, and L-NAME, but not AG nor 7-NI, abolished the protection produced by isoflurane. CONCLUSION: The results suggest that the protective effects of isoflurane against infarction during early reperfusion are mediated by Erk1/2, p70s6K, and eNOS in vivo. |
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Authors:
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John G Krolikowski; Dorothee Weihrauch; Martin Bienengraeber; Judy R Kersten; David C Warltier; Paul S Pagel |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Canadian journal of anaesthesia = Journal canadien d'anesthésie Volume: 53 ISSN: 0832-610X ISO Abbreviation: Can J Anaesth Publication Date: 2006 Feb |
Date Detail:
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Created Date: 2006-01-25 Completed Date: 2006-06-28 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 8701709 Medline TA: Can J Anaesth Country: Canada |
Other Details:
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Languages: eng Pagination: 174-82 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anesthetics, Inhalation
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pharmacology* Animals Extracellular Signal-Regulated MAP Kinases / antagonists & inhibitors, metabolism* Flavonoids / pharmacology Ischemic Preconditioning, Myocardial* Isoflurane / pharmacology* Male Myocardial Reperfusion Injury / metabolism, prevention & control* NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide Synthase Type III / antagonists & inhibitors, metabolism* Rabbits Ribosomal Protein S6 Kinases, 70-kDa / antagonists & inhibitors, metabolism* Sirolimus / pharmacology |
| Grant Support | |
ID/Acronym/Agency:
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GM 008377/GM/NIGMS NIH HHS; GM 066730/GM/NIGMS NIH HHS; HL 054820/HL/NHLBI NIH HHS; HL 063705/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anesthetics, Inhalation; 0/Flavonoids; 0/PD 98059; 26675-46-7/Isoflurane; 50903-99-6/NG-Nitroarginine Methyl Ester; 53123-88-9/Sirolimus; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 2.7.11.1/Ribosomal Protein S6 Kinases, 70-kDa; EC 2.7.11.24/Extracellular Signal-Regulated MAP Kinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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