Effects of stimulation of the cardiac sympathetic nerves and intravenous administration of sympathomimetic amines on the multiple response or fibrillation threshold (VMRT) and on other properties of the dog ventricles were compared. Stimulation of the cardiac sympathetic nerves decreased the VMRT. Administration of sympathomimetic amines caused a brief decrease in the VMRT followed by a sustained increase. Temporal dispersion of recovery of excitability and the degree of ventricular vulnerability were closely related; the ventricle was more vulnerable to fibrillation when the dispersion was increased. The hyperkalemic effect of epinephrine was not responsible for the observed changes in ventricular vulnerability.

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The effect of potassium on the longitudinal muscle-myenteric plexus (LM-MP) preparation from guinea-pig was studied. The strips were exposed to elevated K+ (30 mM, 60 mM, 90 mM, 120 mM or 150 mM). A phasic contraction of the LM-MP was caused by 10 mM K+ or 15 mM K+ followed by an increase of the contractile activity probably due to the increase in acetylcholine release. A higher molarity of K+ produces more marked depolarization in the LM-MP and above 22 mM K+ tetanizing effects were observed. We attempted to demonstrate that opiate-like material could be released when the tissue was exposed to more than 30 mM K+ even though several different neurotransmitters could be liberated by elevated K+ molarities.