Verification of a model for the mechanisms controlling expiratory duration in rabbits under various conditions

A mathematical model for the mechanisms controlling expiratory (E) duration was verified through comparison of its prediction with the relationships between TE and waveform parameters of various input patterns obtained by bilateral, simultaneous electrical stimulation of the largest vagal afferent fibers in vagotomized, paralyzed rabbits at normal or elevated chemical drive under light or deep barbiturate anesthesia. The model accurately reproduced experimental results in each animal and condition; it suggests that in the absence of vagal input (v.i.) an exponentially decaying central activity (phi) prevents inspiratory (I) onset until a time independent threshold (phi thr) is reached; the vagal component of phi results from fixed gain, long time constant (tau = 1.07 +/- 0.03 sec; mean +/- SE for N = 37 for N = 37 animals) temporal summation of expiratory v.i., being unaffected by inspiratory v.i.; central and vagal components share a common mechanism, the same value of tau applying to v.i. integration and to phi decay in the absence of v.i. under all conditions; the amplitude of the central component is proportional to tidal changes in central I activity, independently of the condition studied; and phi thr increases at elevated chemical drive, is unaffected by v.i., and decreases under deep anesthesia.