Calcium responsiveness in canine pacing-induced heart failure.
The specific lesion(s) and potential compensatory alterations of excitation-contraction coupling in heart failure are not clear in detail. We therefore subjected five dogs to 2-5 weeks of rapid ventricular pacing until heart failure developed. Data obtained from these five dogs with pacing-induced heart failure were compared to data from six healthy controls. Under anesthesia, in situ steady state responses of regional contractile function to intracoronary calcium infusion were established. Maximal calcium-activated regional contractile function in dogs with heart failure was 46% less than in controls; calcium sensitivity was unchanged [pCa50 2.55+/-0.31 v 2.82+/-0.17 (+/-s.d.)]. Our data point to a decrease in maximal calcium-activated force and an unchanged calcium sensitivity if an unchanged calcium transient is assumed, or a compensatory increase in calcium sensitivity of failing myocardium if a decreased calcium transient is assumed.
Heusch
G
G
Center of Internal Medicine, University of Essen, School of Medicine, FRG.
Neumann
T
T
D000818:Animals; D002118:Calcium / Q000494:pharmacology*; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects*; D004285:Dogs; D006333:Heart Failure / Q000188:drug therapy*; D006439:Hemodynamics / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects*
D002118:Calcium