| A1 adenosine receptor overexpression decreases stunning from anoxia-reoxygenation: role of the mitochondrial K(ATP) channel. | |
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MedLine Citation:
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PMID: 12061393 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Myocardial A1 adenosine receptor (A1AR) overexpression protects hearts from ischemia-reperfusion injury; however, the effects during anoxia are unknown. We evaluated responses to anoxia-reoxygenation in wild-type (WT) and transgenic (Trans) hearts with approximately 200-fold overexpression of A1ARs. Langendorff perfused hearts underwent 20 min anoxia followed by 30 min reoxygenation. In WT hearts peak diastolic contracture during anoxia was 45+/-3 mmHg, diastolic pressure remained elevated at 18+/-3 mmHg after reoxygenation, and developed pressure recovered to 52+/-4% of pre-anoxia. A1AR overexpression reduced hypoxic contracture to 29+/-4 mmHg, and improved recovery of diastolic pressure to 8+/-1 mmHg and developed pressure to 76+/-3% of pre-anoxia. Mitochondrial K(ATP) blockade with 100 microM 5-hydroxydecanoate (5-HD) increased hypoxic contracture to 73+/-6 mmHg in WT hearts, reduced post-hypoxic recoveries of both diastolic (40+/-5 mmHg) and developed pressures (33+/-3 %). In contrast, 5-HD had no effect on hypoxic contracture (24+/-8 mmHg), or post-hypoxic diastolic (10+/-2 mmHg) and developed pressures (74+/-3%) in Trans hearts. In summary, (i) A1AR overexpression improves myocardial tolerance to anoxia-reoxygenation, (ii) intrinsic mitochondrial K(ATP) channel activation decreases hypoxic contracture and improves functional recovery in wild-type hearts, and (iii) mitochondrial K(ATP) channels do not appear to play a major role in the functional protection from anoxia afforded by A1AR overexpression. |
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Authors:
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Rachael J Cerniway; R Ray Morrison; Anne M Byford; Amy R Lankford; John P Headrick; David G L Van Wylen; G Paul Matherne |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Basic research in cardiology Volume: 97 ISSN: 0300-8428 ISO Abbreviation: Basic Res. Cardiol. Publication Date: 2002 May |
Date Detail:
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Created Date: 2002-06-13 Completed Date: 2002-12-04 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0360342 Medline TA: Basic Res Cardiol Country: Germany |
Other Details:
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Languages: eng Pagination: 232-8 Citation Subset: IM |
Affiliation:
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Department of Pediatrics, University of Virginia Health Sciences Center, Charlottesville 22908, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adenosine Triphosphate
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physiology* Animals Anoxia / physiopathology Decanoic Acids / pharmacology Female Heart / drug effects, physiopathology Hydroxy Acids / pharmacology Male Mice Mice, Transgenic / genetics Mitochondria, Heart / metabolism* Myocardial Stunning / physiopathology* Oxygen / pharmacology Potassium Channels / drug effects, metabolism* Rats Receptors, Purinergic P1 / genetics, metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL 59419/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Decanoic Acids; 0/Hydroxy Acids; 0/Potassium Channels; 0/Receptors, Purinergic P1; 56-65-5/Adenosine Triphosphate; 624-00-0/5-hydroxydecanoic acid; 7782-44-7/Oxygen |
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