Linked Life Data

11486245

Source:http://linkedlifedata.com/resource/pubmed/id/11486245

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2001-8-7
pubmed:abstractText
Cardioprotection by K(ATP) channel openers during ischemia is well documented although ill understood. Proarrhythmic effects may be an important drawback. K(ATP) channel modulation influences neurotransmitter release during ischemia in brain synaptosomes. Therefore, we studied the effects of K(ATP) channel modulation on myocardial noradrenaline release and arrhythmias in ischemic rabbit hearts. Isolated rabbit hearts were perfused according to Langendorff and stimulated. Local electrograms were recorded and K+-selective electrodes were inserted in the left ventricular free wall. Cromakalim (3 microM) or glibenclamide (3 microM) was added 20 min prior to induction of global ischemia. After 15, 20, or 30 min of ischemia, hearts were reperfused and noradrenaline content of the first 100 ml of reperfusate was measured. Cromakalim (n = 16) prevented the second rise of extracellular [K(+)] in accordance with its cardioprotective effect. Cromakalim significantly reduced noradrenaline release after 15 min (mean, 169 +/- SEM 97 pmol/gr dry weight vs. control 941 +/- 278; p < 0.05) and 20 min of ischemia (230 +/- 125 pmol/gr dry wt vs. control 1,460 +/- 433; p < 0.05), but after 30 min of ischemia, the difference in noradrenaline release was no longer significant (cromakalim 2,703 +/- 1,195 pmol/gr dry wt vs. control 5,413 +/- 1,310; p = 0.08). Ventricular fibrillation or ventricular tachycardia occurred in 10 of 13 control hearts (77%) (n = 19), in six of 10 glibenclamide-treated hearts (60%) (n = 15), and in six of 14 cromakalim-treated hearts (43%) (p = NS). Cromakalim significantly accelerated onset of ventricular tachycardia or fibrillation (mean +/- SEM onset after 12.5 +/- 1.6 min ischemia vs. control 16.2 +/- 0.7 min; p < 0.05). Noradrenaline release occurred only in cromakalim-treated hearts with early-onset arrhythmias whereas no noradrenaline release was observed in cromakalim-treated hearts without ventricular tachycardia or fibrillation. Our results show that activation of the K(ATP) channel by cromakalim during ischemia reduces myocardial noradrenaline release and postpones the onset of irreversible damage, contributing to the cardioprotective potential of K(ATP) openers during myocardial ischemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0160-2446
pubmed:author
pubmed:issnType
Print
pubmed:volume
38
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
406-16
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:11486245-Adenosine Triphosphate, pubmed-meshheading:11486245-Animals, pubmed-meshheading:11486245-Arrhythmias, Cardiac, pubmed-meshheading:11486245-Coronary Circulation, pubmed-meshheading:11486245-Cromakalim, pubmed-meshheading:11486245-Female, pubmed-meshheading:11486245-Glyburide, pubmed-meshheading:11486245-Heart, pubmed-meshheading:11486245-Heart Ventricles, pubmed-meshheading:11486245-Hypoglycemic Agents, pubmed-meshheading:11486245-Male, pubmed-meshheading:11486245-Myocardial Ischemia, pubmed-meshheading:11486245-Myocardium, pubmed-meshheading:11486245-Norepinephrine, pubmed-meshheading:11486245-Potassium, pubmed-meshheading:11486245-Potassium Channels, pubmed-meshheading:11486245-Rabbits, pubmed-meshheading:11486245-Time Factors, pubmed-meshheading:11486245-Vasodilator Agents
pubmed:year
2001
pubmed:articleTitle
K(ATP) channel opening during ischemia: effects on myocardial noradrenaline release and ventricular arrhythmias.
pubmed:affiliation
Experimental and Molecular Cardiology Group, Academic Medical Center, University of Amsterdam, The Netherlands. c.a.remme@amc.uva.nl
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't