Computer simulation of ventilatory control by both neural and humoral CO2 signals.

A mathematical model portraying a humoral signal derived from time-dependent variations in arterial carbon dioxide tension (PaCO2) and a neural signal proportional to the metabolic CO2 production was tested by computer simulation. The signals were assumed to enter the central mechanism through afferent pathways connected in reciprocal inhibition. The central mechanism, previously described, contained proportional, gradient, and positive feedback components. The model simulates steady-state isocapnic hyperpnea under endogenous CO2 load and hyperpnea proportional to PaCO2 under exogenous CO2 load. This behavior is consistent whether the neural signal is present alone, the humoral signal is present alone, or both are present and synergistic. When the neural and humoral signals are opposed hypocapnia and hyperventilation ensue; the values being consistent with the isometabolic hyperbola. The model also portrays steady-state behavior when CO2 is inhaled during exercise. During hypometabolic states of rest the mechanism appears to become insensitive to PaCO2 levels.