Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2006-9-19
pubmed:abstractText
We have previously found that uridine 5'-triphosphate (UTP) significantly reduced cardiomyocyte death induced by hypoxia via activating P2Y(2) receptors. To explore the effect of UTP following myocardial infarction (MI) in vivo we studied four groups: sham with or without LAD ligation, injected with UTP (0.44microg/kg i.v.) 30min before MI, and UTP injection (4.4microg/kg i.v.) 24h prior to MI. Left ventricular end diastolic area (LVEDA), end systolic area (LVESA) fractional shortening (FS), and changes in posterior wall (PW) thickness were performed by echocardiography before and 24h after MI. In addition, we measured different biochemical markers of damage and infarct size using Evans blue and TTC staining. The increase in LVEDA and LVESA of the treated animals was significantly smaller when compared to the MI rats (p<0.01). Concomitantly, FS was higher in groups pretreated with UTP 30min or 24h (56+/-14.3 and 36.7+/-8.2%, p<0.01, respectively). Ratio of infarct size to area at risk was smaller in the UTP pretreated hearts than MI rats (22.9+/-6.6, 23.1+/-9.1%, versus 45.4+/-7.6%, respectively, p<0.001). Troponin T and ATP measurements, demonstrated reduced myocardial damage. Using Rhod-2-AM loaded cardiomyocytes, we found that UTP reduced mitochondrial calcium levels following hypoxia. In conclusion, early or late UTP preconditioning is effective, demonstrating reduced infarct size and superior myocardial function. The resulting cardioprotection following UTP treatment post ischemia demonstrates a reduction in mitochondrial calcium overload, which can explain the beneficial effect of UTP.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0006-2952
pubmed:author
pubmed:issnType
Print
pubmed:day
16
pubmed:volume
72
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
949-55
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:16939682-Adenosine Triphosphate, pubmed-meshheading:16939682-Animals, pubmed-meshheading:16939682-Anoxia, pubmed-meshheading:16939682-Blood Pressure, pubmed-meshheading:16939682-Calcium, pubmed-meshheading:16939682-Cardiotonic Agents, pubmed-meshheading:16939682-Cells, Cultured, pubmed-meshheading:16939682-Creatine Kinase, pubmed-meshheading:16939682-Echocardiography, pubmed-meshheading:16939682-Heart, pubmed-meshheading:16939682-Heart Rate, pubmed-meshheading:16939682-Male, pubmed-meshheading:16939682-Mitochondria, pubmed-meshheading:16939682-Myocardial Infarction, pubmed-meshheading:16939682-Myocytes, Cardiac, pubmed-meshheading:16939682-Rats, pubmed-meshheading:16939682-Rats, Wistar, pubmed-meshheading:16939682-Troponin T, pubmed-meshheading:16939682-Uridine Triphosphate
pubmed:year
2006
pubmed:articleTitle
Uridine-5'-triphosphate (UTP) reduces infarct size and improves rat heart function after myocardial infarct.
pubmed:affiliation
The Mina & Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan 52900, Israel.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Intramural