The L-Type Ca+ and KATP channels may contribute to pacing-induced protection against anoxia-reoxygenation in the embryonic heart model.

Details

Serval ID
serval:BIB_1514128B9275
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
The L-Type Ca+ and KATP channels may contribute to pacing-induced protection against anoxia-reoxygenation in the embryonic heart model.
Journal
Journal of Cardiovascular Electrophysiology
Author(s)
Bruchez P., Sarre A., Kappenberger L., Raddatz E.
ISSN
1540-8167[electronic]
Publication state
Published
Issued date
2008
Volume
19
Number
11
Pages
1196-1202
Language
english
Abstract
L-Type Ca(2+) and K(ATP) Channels in Pacing-Induced Cardioprotection. AIMS: The L-type Ca(2+) channel, the sarcolemmal (sarcK(ATP)), and mitochondrial K(ATP) (mitoK(ATP)) channels are involved in myocardial preconditioning. We aimed at determining to what extent these channels can also participate in pacing-induced cardioprotection. METHODS: Hearts of 4-day-old chick embryos were paced in ovo during 12 hour using asynchronous intermittent ventricular stimulation at 110% of the intrinsic rate. Sham operated and paced hearts were then submitted in vitro to anoxia (30 minutes) and reoxygenation (60 minutes). These hearts were exposed to L-type Ca(2+) channel agonist Bay-K-8644 (BAY-K) or blocker verapamil, nonselective K(ATP) channel antagonist glibenclamide (GLIB), mitoK(ATP) channel agonist diazoxide (DIAZO), or antagonist 5-hydroxydecanoate. Electrocardiogram, electromechanical delay (EMD) reflecting excitation-contraction (E-C) coupling, and contractility were determined. RESULTS: Under normoxia, heart rate, QT duration, conduction, EMD, and ventricular shortening were similar in sham and paced hearts. During reoxygenation, arrhythmias ceased earlier and ventricular EMD recovered faster in paced hearts than in sham hearts. In sham hearts, BAY-K (but not verapamil), DIAZO (but not 5-hydroxydecanoate) or GLIB accelerated recovery of ventricular EMD, reproducing the pacing-induced protection. By contrast, none of these agents further ameliorated recovery of the paced hearts. CONCLUSION: The protective effect of chronic asynchronous pacing at near physiological rate on ventricular E-C coupling appears to be associated with subtle activation of L-type Ca(2+) channel, inhibition of sarcK(ATP) channel, and/or opening of mitoK(ATP) channel.
Keywords
Animals, Cardiac Pacing, Artificial/methods, Chick Embryo, Disease Models, Animal, Fetal Hypoxia/metabolism, Fetal Hypoxia/prevention & control, Humans, Ischemic Preconditioning, Myocardial/methods, Myocardial Reperfusion Injury/embryology, Myocardial Reperfusion Injury/metabolism, Myocardium/metabolism, Potassium Channels/metabolism, Treatment Outcome
Pubmed
Web of science
Open Access
Yes
Create date
18/09/2009 15:50
Last modification date
20/08/2019 12:44
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