The L-type Ca2+ and KATP channels may contribute to pacing-induced protection against anoxia-reoxygenation in the embryonic heart model

Journal of Cardiovascular Electrophysiology

Volumn 19, Issue 11, 2008, Pages 1196-1202

  Bruchez, Philippe ^a   Sarre, Alexandre ^a   Kappenberger, Lukas ^b   Raddatz, Eric ^a,c  

^a UNIVERSITY OF LAUSANNE   (Switzerland)

^b LAUSANNE UNIVERSITY HOSPITAL   (Switzerland)

^c UNIVERSITY OF LAUSANNE   (Switzerland)

Author keywords

Anoxia reoxygenation; Asynchronous pacing; Cardioprotection; KATP channels; L type Ca 2+ channel; Mitochondria

Indexed keywords

1,4 DIHYDRO 2,6 DIMETHYL 5 NITRO 4 [2 (TRIFLUOROMETHYL)PHENYL] 3 PYRIDINECARBOXYLIC ACID METHYL ESTER; 5 HYDROXYDECANOIC ACID; CALCIUM CHANNEL L TYPE; DIAZOXIDE; GLIBENCLAMIDE; POTASSIUM CHANNEL; VERAPAMIL;

ANIMAL EXPERIMENT; ANIMAL MODEL; ARTICLE; CHICK; CONTROLLED STUDY; ELECTROCARDIOGRAM; ELECTROMECHANICAL DELAY; EMBRYO; EXCITATION CONTRACTION COUPLING; HEART MUSCLE CONTRACTILITY; HEART MUSCLE ISCHEMIA; HEART PACING; HEART PROTECTION; NONHUMAN; PRIORITY JOURNAL; REOXYGENATION; REPERFUSION INJURY;

ANIMALS; CARDIAC PACING, ARTIFICIAL; CHICK EMBRYO; DISEASE MODELS, ANIMAL; FETAL HYPOXIA; HUMANS; ISCHEMIC PRECONDITIONING, MYOCARDIAL; MYOCARDIAL REPERFUSION INJURY; MYOCARDIUM; POTASSIUM CHANNELS; TREATMENT OUTCOME;

EID: 55449107110     PISSN: 10453873     EISSN: 15408167     Source Type: Journal    
DOI: 10.1111/j.1540-8167.2008.01218.x     Document Type: Article

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