Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1994-1-26
pubmed:abstractText
Tissue injury associated with myocardial ischemia is assumed to largely result from the toxic effects of active oxygen species generated by accumulated polymorphonuclear leukocytes (PMNs). Recent reports have indicated that adenosine can interfere with the PMN function in vitro. The potential of adenosine to influence PMN-mediated myocardial tissue injury was assessed using a model of ischemia-reperfusion injury developed in the isolated working guinea-pig heart perfused with homologous PMNs. After an initial work phase, hearts were subjected to 30 min low-flow ischemia (1 ml/min) in the absence and presence of PMNs. Work was resumed after 15 min reperfusion in a non-working mode (Langendorff). Adenosine in the coronary effluent reached a maximum of 0.2 microM during low-flow ischemia. Recoveries of external heart work and cardiac output were reduced from about 80% to about 40% by PMNs. Infusion of adenosine deaminase (ADA, 5 U/ml), theophylline (50 microM) or the selective A1-antagonist dipropyl-8-cyclopentylxanthine (0.1 microM) prevented this effect. Furthermore, application of adenosine (0.1 microM) in combination with PMNs also resulted in a loss of pump function, even in the absence of a direct ischemic stimulus. The data indicate that adenosine contributes to post-ischemic, PMN-mediated damage in the isolated working guinea-pig heart model by a receptor-mediated action.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-2828
pubmed:author
pubmed:issnType
Print
pubmed:volume
25
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
927-38
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8263962-Adenosine, pubmed-meshheading:8263962-Adenosine Deaminase, pubmed-meshheading:8263962-Animals, pubmed-meshheading:8263962-Blood Flow Velocity, pubmed-meshheading:8263962-Cardiac Output, pubmed-meshheading:8263962-Coronary Circulation, pubmed-meshheading:8263962-Disease Models, Animal, pubmed-meshheading:8263962-Guinea Pigs, pubmed-meshheading:8263962-Heart, pubmed-meshheading:8263962-Heart Rate, pubmed-meshheading:8263962-Lactates, pubmed-meshheading:8263962-Male, pubmed-meshheading:8263962-Myocardial Ischemia, pubmed-meshheading:8263962-Myocardial Reperfusion, pubmed-meshheading:8263962-Myocardial Reperfusion Injury, pubmed-meshheading:8263962-Neutrophils, pubmed-meshheading:8263962-Receptors, Purinergic P1, pubmed-meshheading:8263962-Theophylline, pubmed-meshheading:8263962-Xanthines
pubmed:year
1993
pubmed:articleTitle
Adenosine contributes to neutrophil-mediated loss of myocardial function in post-ischemic guinea-pig hearts.
pubmed:affiliation
Department of Physiology, University of Munich, Germany.
pubmed:publicationType
Journal Article, In Vitro