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This experiment extends Pavlov's method of contrasts for training a stimulus discrimination to the case of the cardiac conditional response in the rhesus monkey. It explores the parameter of temporal placement of an additional stimulus ("CS2") within a 10-sec CS (or "CS1"), with the appearance of the former stimulus on any trial signalling the absence of UCS (electric shock) on that trial. This experimental paradigm is a parallel to that of the "intruded stimulus" studies in operant conditioning. In both cases, several ways of describing the function of the added stimulus are possible, but all seem reducible to the same operational terms. Data were taken in the present study with respect to the form and latency of the cardiac rate changes produced by intrusion of CS2 (light), across a range of placements varying from simultaneity with CS1 (a different light) onset to two sec before UCS would have been delivered. The control of CS2 over the cardiac rate CR was occasionally exhibited with a latency as short as three beats after stimulus onset. The order of CS2 temporal placements to which a subject was exposed was a factor in determining the form of the conditioned cardiac rate response to CS1.

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.