125.
This communication compares the well known phenomenon of respiratory driving by the respiratory pump through the Breuer Hering reflex with a model (
Segundo, 1979) of a neuronal pacemaker (i.e. regularly firing) interactions via
IPSP's. The assumption involves a linear dependence (“delay function”) of the postsynaptic interval lengthening (or “delay”) produced by the
IPSP's on the position (or “phase”) with respect to the preceding spike of the latter's arrival. Cats anesthetized and paralized with gallamine were artificially ventilated using a computer driven respirator. The pump period and the respiratory period (identified by the phrenic discharge) corresponded to the model's presynaptic pacemaker interval and to that of the post synaptic one, respectively. The delay of the respiratory period by an inflation was related linearly and in increasing manner to the latter's phase with respect to the inspiration onset. In the steady state, plots of average respiratory period versus pump period consisted in a succession of broad “paradoxical” segments with positive slopes 3, 2, 1, 1/2, 1/3 in which respiration was locked with the pump as predicted by the model. The locked condition were less easy to reach when F
A CO 2increased or when level of anaesthesia decreased. The limits of paradoxical segments were different when measured using pump periods that increased or using periods that decreased. There was therefore a hysteresis as if the delay function parameters changed, a behavior that was not part of the model that assumed fixed characteristics. These modifications were related to dependency of each cycle on the preceding one. The model proposed for simple neuronal pacemaker interactions can thus be applied satisfactorily to the drive of the complex respiratory neuronal oscillator by the respiratory pump through Breuer Hering reflex, providing nevertheless some additonal assumptions concerning respiratory cycle interdependency are introduced to account for the hysteresis phenomenon. The Breuer Hering reflex could be considered as the equivalent of
IPSP acting on the central respiratory oscillator. F
A CO 2increase and anesthesia level decrease produced the same effect as the addition of noise to the model's presynaptic pacemaker, thus leading to the hypothesis that they act by adding noise (e.g., randomly distributed excitatory input) at the level of Breuer Hering reflex inhibition.
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