Abstract
The excised atrio-ventricular septum of a rabbit's heart and a papillary muscle and its attached false tendon from a dog's heart were used in order to study the effects of calcium deficiency on the propagation of impulses through the mammalian heart junctional regions. The preparations were isolated and perf used with aerated flowing Tyrode solutions. The transmembrane potentials of the different cardiac cells were recorded through conventional technics.
The perfusion with calcium-free solutions produced, within variable periods of time, a decrease in RMP, rate of rise and amplitude of action potentials. An increase in duration of the responses preceded the former changes. The sensitivity of the explored cardiac tissues to the lack of calcium varied, the Purkinje fiber response being the most modified (FIG. 1). All changes produced by calcium deficiency were reversible (FIG. 2).
The propagation of impulses through the A.V. node junctional regions was slowed and in some cases blocked (FIGS. 3, 4 and 5A). These effects were more evident and appeared earlier in the fibers joining the lower part of A.V. node and the bundle of His (N-H) than in the auricle-A.V. node junctional region (A-N). Similar effects were observed in the Purkinjemyocardial cells junction (FIG. 6) in which calcium deficiency changed in a greater proportion the propagation of the impulses travelling from Purkinje to myocardial fibers (P-M) than that in the opposite direction (M-P).
The changes in propagation were reverted by adding calcium either to the perfusing chamber or through a micropipette subjected to hydrostatic pressure and placed on the junctional region (FIGS. 5B, C and 7).
The results show that the outstanding effects of the calcium-free solutions on the junctional regions may be due mainly to modifications produced on the membranes of transitional cells generating “transitional potentials”. These modifications would be produced indirectly acting through the sodium ions carrying system.
