Coraboeuf E, Coulombe A, Deroubaix E, Hatem S, Mercadier J J
Laboratoire de Cardiologie Cellulaire et Moléculaire, CNRS ERS 566, Hôpital Marie Lannelongue, Le Plessis Robinson.
Bull Acad Natl Med. 1997 Jun-Jul;181(6):1143-50; discussion 1150-1.
Several studies have shown that the Na-Ca exchange is electrogenic in cardiac tissues and that the current carried by the exchange, iNa-Ca, participates in the development of the cardiac action potential plateau. The aim of the present study was to assess the contribution of iNa-Ca to the development of the plateau in different preparations, i.e. normal and hypertrophied (DOCA-salt) perfused rat hearts, normal and dilated (MS 200 strain) perfused hamster hearts and normal human atrial myocytes and to examine the repercussion of iNa-Ca suppression on the global electrogram of the perfused guinea-pig heart. iNa-Ca was suppressed by briefly substituting lithium for sodium (Li test). In the normal rat heart, the Li test resulted in a depression of the late component of the plateau. In the severely hypertrophied rat heart, the action potential was lengthened, the two components of the plateau barely distinguishable. The part of the plateau suppressed during Li perfusion was not larger in amplitude than in the normal rat heart, but was of much longer duration. In the dilated heart of hamsters older than 60 days of age the shortening effect of the Li test was much larger than in the normal hamster heart indicating a strongly increased contribution of iNa-Ca to the plateau development during dilatation. The contribution of iNa-Ca to the action potential plateau of human atrial myocytes was as large as that found in animal ventricles and varied with the type of cell studied. In the perfused guinea-pig heart the Li test resulted in a sizeable shortening of QT duration and a marked decrease in T wave amplitude suggesting that iNa-Ca may be a major source of current in the building up of the ventricular complex of the electrocardiogram in normal and pathological conditions.
