HOMEPRODUCTSCOMPANYCONTACTFAQResearchDictionaryPharmaSign Up FREE or Login

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

AbstractUNLABELLED:
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.
AuthorsPhilippe Bruchez, Alexandre Sarre, Lukas Kappenberger, Eric Raddatz
JournalJournal of cardiovascular electrophysiology (J Cardiovasc Electrophysiol) Vol. 19 Issue 11 Pg. 1196-202 (Nov 2008) ISSN: 1540-8167 [Electronic] United States
PMID18554212 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Potassium Channels
  • mitochondrial K(ATP) channel
Topics
  • Animals
  • Cardiac Pacing, Artificial (methods)
  • Chick Embryo
  • Disease Models, Animal
  • Fetal Hypoxia (metabolism, prevention & control)
  • Humans
  • Ischemic Preconditioning, Myocardial (methods)
  • Myocardial Reperfusion Injury (embryology, metabolism, prevention & control)
  • Myocardium (metabolism)
  • Potassium Channels (metabolism)
  • Treatment Outcome

Join CureHunter, for free Research Interface BASIC access!

Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find out why thousands of doctors, pharma researchers and patient activists around the world use CureHunter every day.
Realize the full power of the drug-disease research graph!


Choose Username:
Email:
Password:
Verify Password:
Enter Code Shown: