Abstract
The perfused heart in situ and strip preparations were used. In the in situ preparation, low-Na hypoosmotic saline had a positive inotropic effect, shortened the A-V interval and abolished arrhythmia or A-V blocking. The return to normal saline caused a transient offresponse: further acceletation of the heartbeat and further shortening of the A-V interval. Low-Na isoosmotic saline (sodium replaced by sucrose) increased pacemaker activity but the effect on the length of the A-V interval was variable. In the strip preparation, Low-Na hypoosmotic saline increased the rate of rise of the action potentials of atrioventricular ring (R-potentials) and shortened its latency of activation. The effects of the isoosmotic saline varied with the substitute used, either sucrose or lithium. Sucrose saline gave unpredictable results, though the rate of rise of R-potentials increased in 14 out of 24 experiments. Lithium saline decreased the rate of rise of R-potentials and blocked atrioventricular propagation in all experiments. Tetrodotoxin (10-5g/ml) did not abolish R-potentials. An increase of calcium concentration to 3 and 5 times the normal decreased the rate of rise of R-potentials and blocked atrio-ventricular propagation. While the Low-Na saline blocked pacemaker activity at the sinus venosus, it stimulated the generation of R-potentials, so that throughout low-Na treatment, the site of pacemaker activity shifted to the A-V ring. The situation was reversed when normal saline was restored. The data are discussed according to the current ideas of action potential generation.
