Document Detail


A1 adenosine receptor overexpression decreases stunning from anoxia-reoxygenation: role of the mitochondrial K(ATP) channel.
MedLine Citation:
PMID:  12061393     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Basic research in cardiology     Volume:  97     ISSN:  0300-8428     ISO Abbreviation:  Basic Res. Cardiol.     Publication Date:  2002 May 
Date Detail:
Created Date:  2002-06-13     Completed Date:  2002-12-04     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0360342     Medline TA:  Basic Res Cardiol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  232-8     Citation Subset:  IM    
Affiliation:
Department of Pediatrics, University of Virginia Health Sciences Center, Charlottesville 22908, USA.
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MeSH Terms
Descriptor/Qualifier:
Adenosine Triphosphate / 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:
R01 HL 59419/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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