Document Detail


Coronary function and adenosine receptor-mediated responses in ischemic-reperfused mouse heart.
MedLine Citation:
PMID:  12062719     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVES: To assess the impact of ischemia-reperfusion (I/R) on coronary function, and the role of endogenous adenosine in modifying post-ischemic vascular function in asanguinous hearts. METHODS: Vascular function was studied in Langendorff perfused mouse hearts subjected to 20-25-min ischemia and 30-min reperfusion. RESULTS: Ischemia altered the dependence of flow on work-rate observed in normoxic hearts, and inhibited reflow by mechanisms additional to diastolic compression. Coronary responses were selectively reduced: 2-chloroadenosine and ADP dilated with pEC(50)s of 8.4+/-0.1 and 7.4+/-0.1 in non-ischemic hearts versus 7.7+/-0.1 and 7.1+/-0.1 after 20-min ischemia (P<0.05). Sensitivity was further reduced after 25-min ischemia. Responses to nitroprusside were unaltered. NO-synthase antagonism (50 microM nitro-L-arginine methylester) reduced sensitivities to 2-chloroadenosine and ADP up to 10-fold, and eliminated inhibitory effects of I/R. K(ATP) blockade with 5 microM glibenclamide impaired sensitivity pre- and post-ischemia, not eliminating the inhibitory effects of I/R. A(1) adenosine receptor antagonism with 100 nM 8-cyclopentyl-1,3-dipropylxanthine worsened effects of ischemia on sensitivity. A(2A) adenosine receptor antagonism with 100 nM 8-(3-chlorostyryl)caffeine reduced post-ischemic flow by 50%, yet paradoxically enhanced post-ischemic contractile recovery. CONCLUSIONS: Ischemia modifies vascular control and impairs NO- versus K(ATP)-dependent coronary dilation in an asanguinous model. Endogenous adenosine protects against vascular dysfunction via A(1) receptors, and determines coronary reflow via A(2A) receptors. However, intrinsic A(2A) activation apparently worsens contractile dysfunction.
Authors:
Amanda J Flood; Laura Willems; John P Headrick
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Cardiovascular research     Volume:  55     ISSN:  0008-6363     ISO Abbreviation:  Cardiovasc. Res.     Publication Date:  2002 Jul 
Date Detail:
Created Date:  2002-06-13     Completed Date:  2002-09-06     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0077427     Medline TA:  Cardiovasc Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  161-70     Citation Subset:  IM    
Affiliation:
Heart Foundation Research Centre, School of Health Science, Griffith University Gold Coast Campus, Southport, Qld 4217, Australia.
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MeSH Terms
Descriptor/Qualifier:
2-Chloroadenosine / pharmacology
Adenosine / analogs & derivatives*,  pharmacology
Adenosine Diphosphate / pharmacology
Animals
Caffeine / analogs & derivatives*,  pharmacology
Coronary Circulation
Heart / physiopathology*
Male
Mice
Mice, Inbred C57BL
Models, Animal
Myocardial Contraction
Myocardial Reperfusion Injury / physiopathology*
Nitroprusside / pharmacology
Perfusion
Phenethylamines / pharmacology
Receptors, Purinergic P1 / antagonists & inhibitors
Vasodilator Agents / pharmacology
Xanthines / pharmacology
Grant Support
ID/Acronym/Agency:
HL 59419/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Phenethylamines; 0/Receptors, Purinergic P1; 0/Vasodilator Agents; 0/Xanthines; 102146-07-6/1,3-dipropyl-8-cyclopentylxanthine; 120225-54-9/CGS 21680; 146-77-0/2-Chloroadenosine; 148589-13-3/8-(3-chlorostyryl)caffeine; 15078-28-1/Nitroprusside; 58-08-2/Caffeine; 58-61-7/Adenosine; 58-64-0/Adenosine Diphosphate

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