Abstract
The functional relationship between heart rate, under atrial pacing, and the intensity of pacing pulses, was determined for intensities ranging from well below the complete heart rate capture threshold to suprathreshold intensities. A separate capture-intensity function was determined for each of the pacing frequencies 180, 240, 300 and 360 pulses per min, and then used to evaluate the effects of propranolol hydrochloride and atropine sulfate on atrial pacing. Propranolol resulted in an increase in the amount of current (mA) required to achieve a given degree of cardiac capture, whereas atropine resulted in a decrease. These shifts in the capture-intensity functions along the intensity axis were possibly caused by drug antagonism of beta-adrenergic and cholinergic receptors, respectively, although the effects might also have been due to modifications of the electrical responsivity of the cardiac muscle, independently of the neural blockade.
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