Journal of Applied Physiology, Vol 50, Issue 4 835-843, Copyright © 1981 by American Physiological Society
Computer simulation of experiments in responses to intravenous and inhaled CO2
W. S. Yamamoto
A simulation of ventilatory responses to infused and inhaled CO2 at
controlled cardiac output and high and low levels of neural excitation
mimics comparable experiments in animals. The model suggests that at low
levels of endogenous and exogenous CO2 load the alert quiescent animal will
show hyperpnea to both test states associated with hypercapnia. The
nonalert quiescent animal simulated will show an isocapnic response to
endogenous load and hypercapnic response to exogenous load. The explanation
of this behavior lies in the model formulation, which allows the neural
signal from metabolically active sources to drive the proportional
component of the controller below an operating level established by its set
point. By this reasoning the excited but metabolically inactive animal
should be paradoxically less sensitive to small changes in CO2, whether
exogenous or endogenous, than the quiescent animal. The model demonstrates
further that a neural "exercise" signal in proportion to venous return
better simulates observations in which CO2 load and venous return are
dissociated than one in which the neural signal is computed from
metabolism. The use of delta V/delta P slopes as estimates of sensitivity
go awry in experiment and simulation when blood flow, CO2 level, and neural
excitatory state are dissociated. This is particularly true when the
organism is operating at and below the hypothesized set point.
