Document Detail


A(3) adenosine receptor activation attenuates neutrophil function and neutrophil-mediated reperfusion injury.
MedLine Citation:
PMID:  10564145     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
This study tested the hypothesis that A(3) adenosine receptors inhibit neutrophil (PMN) function and PMN-mediated reperfusion injury. 2-Chloro-N(6)-(3-iodobenzyl)adenosine-5'-N-methyluronamide (Cl-IB-MECA), an A(3) agonist, did not attenuate superoxide production or myeloperoxidase release from stimulated PMNs. However, Cl-IB-MECA reduced platelet-activating factor-stimulated PMN adherence to coronary endothelium at low concentrations: 52 +/- 27, 45 +/- 10, and 87 +/- 23 PMNs/mm(2) at 0.1, 1.0, and 10 nM vs. 422 +/- 64 PMNs/mm(2) with platelet-activating factor alone. This inhibition was not blocked by A(1) (5 microM KW-3902) or A(2a) (5 microM KF-21326) antagonists: 44 +/- 3 and 43 +/- 2 PMNs/mm(2), respectively. Endothelial pretreatment with 1 nM Cl-IB-MECA reduced PMN adherence, which was reversed by the A(3) antagonist MRS-1220 (100 nM). PMN-mediated reperfusion injury was initiated in isolated rabbit hearts by infusion of 28 x 10(6) PMNs/min for 10 min early in reperfusion. PMNs caused a significant decrease in recovery of left ventricular developed pressure and positive and negative time derivatives of pressure (23 +/- 3, 25 +/- 3, and 23 +/- 3% of baseline, respectively) vs. buffer-perfused hearts (43 +/- 7, 44 +/- 7, and 45 +/- 6%, respectively). Cl-IB-MECA (10 nM) given at reperfusion attenuated the PMN-mediated loss of contractile recovery (40 +/- 3, 46 +/- 5, and 42 +/- 4% of baseline). Cl-IB-MECA reduced myeloperoxidase release activity (5.3 +/- 0.6 absorbance units/min) and CD18-positive cells (54 +/- 9 cells/slide) compared with the untreated PMN group (17.9 +/- 1.7 absorbance units/min and 183 +/- 68 cells/slide). We conclude that Cl-IB-MECA attenuates reperfusion injury by decreasing PMN-endothelial cell interactions. These results suggest that the A(3) adenosine receptor may be a novel therapeutic target for treatment of myocardial ischemia and reperfusion.
Authors:
J E Jordan; V H Thourani; J A Auchampach; J A Robinson; N P Wang; J Vinten-Johansen
Related Documents :
3263835 - Effects of amodiaquine, chloroquine, and mefloquine on human polymorphonuclear neutroph...
2155275 - Effect of idarubicin and epirubicin on in vitro polymorphonuclear function: diminished ...
2995525 - Modulation of neutrophil-reduced pyridine nucleotide content following stimulation with...
16631375 - Glycyrrhizin inhibits neutrophil-associated generation of alternatively activated macro...
11336625 - Atorvastatin.
2207005 - The platelet and plasma pools of plasminogen activator inhibitor (pai-1) vary independe...
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:  The American journal of physiology     Volume:  277     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1999 Nov 
Date Detail:
Created Date:  1999-12-20     Completed Date:  1999-12-20     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1895-905     Citation Subset:  IM    
Affiliation:
Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Crawford Long Hospital of Emory University, Atlanta, Georgia 30365, USA. jjordan@zeus.bwh.harvard.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Animals
Arteries / metabolism,  physiology
Binding, Competitive
COS Cells
Cell Adhesion
Cell Degranulation
Coronary Vessels / metabolism,  physiology
Dogs
Hemodynamics
Myocardial Contraction
Myocardial Reperfusion Injury / metabolism,  physiopathology*
Myocardium / enzymology
Neutrophils / physiology*
Peroxidase / metabolism
Rabbits
Receptors, Purinergic P1 / metabolism,  physiology*
Superoxides / metabolism
Ventricular Function, Left
Grant Support
ID/Acronym/Agency:
N01 MH-30003/MH/NIMH NIH HHS
Chemical
Reg. No./Substance:
0/Receptors, Purinergic P1; 11062-77-4/Superoxides; EC 1.11.1.7/Peroxidase

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


Previous Document:  Role of endothelin-1 in age-dependent cerebrovascular hypotensive responses after brain injury.
Next Document:  Age-related left ventricular function in the mouse: analysis based on in vivo pressure-volume relati...