In 6 ourarized dogs, the magnitudes of both the cardiac acceleration during shock stimulation and deceleration after stimulation were found to be (a) monotonic increasing functions of intensity (2, 4, 6, and 8 ma.) and (b) inverted U-shaped functions of duration (0.1, 0.5, 2.5, 5.0, and 10.0 sec.) of electric shock. Utilizing 32 curarized dogs with a discriminative classical conditioning procedure, (a) the presence of a warning signal did not affect the magnitude of the unconditioned cardiac response, and (b) previous experience with shocks of lower intensity did reduce the magnitude of the unconditioned cardiac response to subsequent high-intensity shock.A strong electric shock results in large changes in the dog's heart rate. During shock, heart rate increases abruptly; when shock is terminated, the heart .rate rapidly decreases to a rate below the preshock rate and then slowly returns to normal (Black, Carlson, & Solomon, 1962). The acceleratory phase has been thought to reflect subjective "shock severity," while the deceleratory phase has been thought to reflect subjective "relief." The purpose of our first experiment was to evaluate the degree to which these two cardiac phenomena could usefully serve as indices of severity of electric shock. The purpose of the second experiment was to evaluate the effects of prior experience with shocks of increasing intensity, and the presence of a warning signal on the cardiac indices of shock severity. Both experiments used dogs paralyzed by tubocurarine chloride in order to eliminate movements and to control respiration, two sources of variability which affect heart rate (Westcott & Huttenlocher, 1961).EXPERIMENT 1 Our initial assumption was that the severity of pain is positively related to both

Curarized and subjected 12 normal and cardiac sympathectomized dogs to either signaled or unsignaled shocks. The unsignaled shocks were of several intensities and durations. There were no differences between signaled and unsignaled shocks in their effects on heart-rate, systolic, and diastolic blood-pressure responses. Following the termination of shocks shorter than 5 sec., and during shocks longer than 5 sec., heart rate decreased while blood-pressure indices increased. Heart rate fell below base-line levels directly after stimulus termination although blood-pressure indices were still elevated. This deceleratory overshoot increased over trials of signaled shock in all sympathectomized Ss. Such functional differences between heart rate and blood pressure preclude the strong inference that heart rate is a direct measure of sympathetic activation. (29 ref.)