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A mathematical model of short-term arterial pressure control by the carotid baroreceptors in vagotomized subjects is presented. It includes an elastance variable description of the left and right heart, the systemic and pulmonary circulations, the afferent carotid baroreceptor pathway, a central elaboration unit, and the action of five effector mechanisms. Simulation results suggest that the carotid baroreflex is able to significantly modulate the cardiac function curve, but this effect is masked in vivo by changes in arterial pressure and atrial pressure. During heart pacing, cardiac output increases with frequency at moderate levels of heart rate, then fails to increase further due to a reduction in stroke volume. Shifting from nonpulsatile to pulsatile perfusion of the carotid sinuses decreases the overall baroreflex gain. Finally, a sensitivity analysis suggests that venous unstressed volume control plays the major role in the early hemodynamic response to acute hemorrhage, whereas systemic resistance control is less important. In all cases, there has been satisfactory agreement between model and experimental results.
Mauro Ursino (Thu,) studied this question.