A mathematical model of short-term arterial pressure control by the carotid
baroreceptors in vagotomized subjects is presented, It includes an elastan
ce variable description of the left and right heart, the systemic and pulmo
nary circulations, the afferent carotid baroreceptor pathway, a central ela
boration unit, and the action of five effector mechanisms.
Simulation results suggest that the carotid baroreflex is able to significa
ntly 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, t
hen 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 hemodyna
mic response to acute hemorrhage, whereas systemic resistance control is le
ss important. In all cases, there has been satisfactory agreement between m
odel and experimental results.