The direct injection of cardiac glycosides into the atrioventricular (A-V) node artery of the dog resulted in the appearance of various arrhythmias and conduction disturbances originating in the junctional tissues of the heart. Three short-acting preparations were studied: acetyl-strophanthidin, digoxin, and desacetyllanatoside C, in doses of 1, 5, 10, and 25 μg. Latency of onset, within 4 min, and duration of effect, usually less than 3 h, appeared to depend upon the concentration of glycoside injected. Impaired conduction, ranging from simple PR lengthening to complete A-V block, was obtained with all three substances. A-V nodal tachycardia was seen in a limited number of dogs after acetylstrophanthidin only. The effects of acetylstrophanthidin on A-V propagation were unmodified by atropine pretreatment. However, an enhanced response to vagus nerve stimulation, as well as to intranodally injected acetylcholine, was demonstrated. In addition, acetylstrophanthidin decreased the amount of A-V nodal acceleration obtained from left stellate ganglion stimulation.