Linked Life Data

16679400

Source:http://linkedlifedata.com/resource/pubmed/id/16679400

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-9-15
pubmed:abstractText
To examine ischemic tolerance in the absence of A(1) adenosine receptors (A(1)ARs), isolated wild-type (WT) and A(1)AR knockout (A(1)KO) murine hearts underwent global ischemia-reperfusion, and injury was measured in terms of functional recovery and efflux of lactate dehydrogenase (LDH). Hearts were analyzed by real-time RT-PCR both at baseline and at intervals during ischemia-reperfusion to determine whether compensatory expression of other adenosine receptor subtypes occurs with either A(1)AR deletion and/or ischemia-reperfusion. A(1)KO hearts had higher baseline coronary flow (CF) and left ventricular developed pressure (LVDP) than WT hearts, whereas heart rate was unchanged by A(1)AR deletion. After 20 min of ischemia, CF was attenuated in A(1)KO compared with WT hearts, and this reduction persisted throughout reperfusion. Final recovery of LVDP was decreased in A(1)KO hearts (54.4 +/- 5.1 vs. WT 81.1 +/- 3.4% preischemic baseline) and correlated with higher diastolic pressure during reperfusion. Postischemic efflux of LDH was greater in A(1)KO compared with WT hearts. Real-time RT-PCR demonstrated the absence of A(1)AR transcript in A(1)KO hearts, and the message for A(2A), A(2B), and A(3) adenosine receptors was similar in uninstrumented A(1)KO and WT hearts. Ischemia-reperfusion increased A(2B) mRNA expression 2.5-fold in both WT and A(1)KO hearts without changing A(1) or A(3) expression. In WT hearts, ischemia transiently doubled A(2A) mRNA, which returned to preischemic level upon reperfusion, a pattern not observed in A(1)KO hearts. Together, these data affirm the cardioprotective role of A(1)ARs and suggest that induced expression of other adenosine receptor subtypes may participate in the response to ischemia-reperfusion in isolated murine hearts.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
291
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H1875-82
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16679400-Animals, pubmed-meshheading:16679400-Coronary Vessels, pubmed-meshheading:16679400-Female, pubmed-meshheading:16679400-Gene Deletion, pubmed-meshheading:16679400-Gene Expression Regulation, pubmed-meshheading:16679400-Lactate Dehydrogenases, pubmed-meshheading:16679400-Male, pubmed-meshheading:16679400-Mice, pubmed-meshheading:16679400-Mice, Knockout, pubmed-meshheading:16679400-Myocardial Contraction, pubmed-meshheading:16679400-Myocardial Ischemia, pubmed-meshheading:16679400-Myocardium, pubmed-meshheading:16679400-RNA, Messenger, pubmed-meshheading:16679400-Receptor, Adenosine A1, pubmed-meshheading:16679400-Receptor, Adenosine A2A, pubmed-meshheading:16679400-Receptor, Adenosine A2B, pubmed-meshheading:16679400-Receptor, Adenosine A3, pubmed-meshheading:16679400-Regional Blood Flow, pubmed-meshheading:16679400-Reperfusion Injury, pubmed-meshheading:16679400-Vasodilation
pubmed:year
2006
pubmed:articleTitle
Effects of targeted deletion of A1 adenosine receptors on postischemic cardiac function and expression of adenosine receptor subtypes.
pubmed:affiliation
Division of Critical Care Medicine, St. Jude Children's Research Hospital, 332 N. Lauderdale St., MS 734, Memphis, TN 38105, USA. ray.morrison@stjude.org
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural