Abstract
Summary
The effect of aconitine on the primary properties of heart muscle has been studied in the cold-blooded heart. Its constant action was to increase the rate of spontaneous beating or to initiate a spontaneous rhythm in driven ventricular strips. This action appeared to be independent of change in resting excitability and to result from enhancement of intrinsic rhythmicity. Vagal action on the auricle depressed the pacemaker, decreased contraction amplitude and shortened refractory period. Contractility and refractory period changes were independent of rate change. In the atropinized auricle high concentrations shortened refractory period by direct muscle action. During the stage of shortened refractory period there was a critical interval when a single extra shock might elicit multiple responses. In the turtle ventricle, which has no vagal endings, high concentrations shortened refractory period, decreased conduction velocity and raised threshold for electrical stimulation.
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