Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1999-4-21
pubmed:abstractText
1. Ischaemic preconditioning (IP) can significantly reduce the extent of infarct size, contractile dysfunction and necrosis in hearts from a number of animal species. Activation of ATP-sensitive potassium channels has been implicated in this process. The aims of the present study were to determine the extent to which IP preserves haemodynamic function in the rat isolated working heart model after prolonged hypothermic storage and to examine the involvement of activation of potassium channels in this process. 2. Hearts from Wistar rats were perfused on a Langendorff apparatus. After stabilization in working mode, baseline measurements of heart rate, aortic flow, coronary flow and cardiac output were performed. Hearts were randomized to one of six treatment groups: (i) untreated control; (ii) IP; (iii) 3 min perfusion with 200 mumol/L pinacidil; (iv) pinacidil vehicle; (v) 3 min perfusion with 10 mumol/L glibenclamide before IP; and (vi) 3 min perfusion with glibenclamide then pinacidil. Hearts were stored in an extracellular-based preservation solution for 6 or 12 h at 2-3 degrees C, remounted on the perfusion apparatus, stabilized as before and then haemodynamic measurements were repeated, after which time heart water contents were determined. 3. Recovery of haemodynamic function was markedly enhanced in the IP and pinacidil-treated groups compared with untreated and vehicle controls. These beneficial effects were completely blocked by glibenclamide. These results suggest that strategies for activating potassium channels in donor hearts may protect organs during hypothermic storage prior to transplantation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0305-1870
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
20-5
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10027065-Adenosine Triphosphate, pubmed-meshheading:10027065-Animals, pubmed-meshheading:10027065-Cardioplegic Solutions, pubmed-meshheading:10027065-Glyburide, pubmed-meshheading:10027065-Heart Rate, pubmed-meshheading:10027065-Hemodynamics, pubmed-meshheading:10027065-Hypoglycemic Agents, pubmed-meshheading:10027065-Ischemic Preconditioning, Myocardial, pubmed-meshheading:10027065-Male, pubmed-meshheading:10027065-Organ Preservation, pubmed-meshheading:10027065-Organ Preservation Solutions, pubmed-meshheading:10027065-Pinacidil, pubmed-meshheading:10027065-Potassium Channel Blockers, pubmed-meshheading:10027065-Potassium Channels, pubmed-meshheading:10027065-Rats, pubmed-meshheading:10027065-Rats, Wistar, pubmed-meshheading:10027065-Vasodilator Agents, pubmed-meshheading:10027065-Water
pubmed:year
1999
pubmed:articleTitle
ATP-sensitive potassium channel activation mimics the protective effect of ischaemic preconditioning in the rat isolated working heart after prolonged hypothermic storage.
pubmed:affiliation
Division of Clinical Pharmacology and Toxicology, St Vincent's Hospital, Darlinghurst, New South Wales, Australia. pmacdonald@stvincents.com.au
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't