Effects of Barium on Mature and Embryonic Heart Cells
Barium chloride was administered to isolated preparations of dog heart and rat atrium and to trypsinized embryonic chick heart cells cultured in vitro. Transmembrane action potentials recorded from pacemaker, specialized conductive and contractile fibers of the dog heart, and atrial fibers of rat heart showed a slowing in the rising and falling phases of the action potential and a prominent negative after-potential. The action potential of the Purkinje fiber of the dog heart showed in addition a depolarization during diastole. A decrease in resting potential was observed later.
The isometric tension developed by the rat atrium showed a significant increase which was greater at the higher concentractions (greater than 3.5 x 10-4M) of barium chloride. The cultured embryonic heart cells were appreciably more sensitive to barium than the mature heart cells. An increase in rate of beat of the embryonic heart cells was observed at concentrations of 10-6M whereas a change in heart rate was first observed in the adult heart at concentrations above 10-4M. The induction of beating in cell communities previously quiescent is due to a local automatic activity rather than to a propagated activity from an adjacent cell community.
The slowing in rise time of the action potential can be attributed to a depression of the sodium-carrying system. The slowing of repolarization can be ascribed to a decrease in potassium conductance. The pronounced negative after-potential can be explained on the basis of sustained impermeability of the membrane to potassium. The mechanism by which barium produces a positive inotropic effect in the rat atrium is open to conjecture. It cannot be attributed solely to a prolongation of the duration of the action potential nor can a direct effect on the contractile proteins be excluded. The presence of extracellular calcium is essential in order to obtain a positive inotropic effect in the rat atrium when barium is added.
- Accepted October 25, 1965.
- © 1966 American Heart Association, Inc.