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Intra-atrial, intranodal and His-Purkinje conduction times were determined in perfused rabbit hearts. In one series, the concentration of lanatoside C was increased by 0.4 mg/liter every 30 minutes, in the presence of normal (4.5) or high (7.5 mM) K+ in the perfusion fluid. At high (K+) the glycoside produced a greater increase in intra-atrial and His-Purkinje conduction times but caused a smaller increase of intranodal conduction time than at normal (K+). Second-degree A-V block always occurred intranodally, but the incidence was lower with high (K+). In another series, (K+) was increased by 3 mM every 30 minutes, in the absence or presence (0.4, 0.8 or 1.2 mg/liter) of lanatoside C. No difference was seen between hearts treated with lanatoside C and those untreated at the level of (K+) producing failure of conduction. At all levels of glycoside, conduction delay caused by high (K+) was greatest within the atria, less in the His-Purkinje system and insignificant within the A-V node. Intra-atrial and His Purkinje block were observed but never an intranodal block. It is concluded that (1) cardiac glycoside and high (K+) primarily affect different regions of the A-V conducting system, and (2) aggravation of glycoside-induced A-V block by high (K+) may result from additional intra-atrial and His-Purkinje block rather than from further depression of intranodal conduction. Electrophysiological mechanisms underlying these interactions were also discussed.

Interactions of Lanatoside C and Potassium on Atrioventricular Conduction in Rabbits