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International Conference on Mathematical Biology and

Annual Meeting of The Society for Mathematical Biology,

July 27-30, 2009

University of British Columbia, Vancouver

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Program

MSD4c
Alona Ben-Tal
Institute of Information and Mathematical Sciences, Massey University
Title Circulatory Delay Vs. Neural Feedback Dynamics
Abstract We used a recently developed mathematical model of the control of breathing to study numerically how circulatory time delay and the dynamics of neural feedback affect the response of the respiratory system to hypercapnia and hypoxia as well as the appearance of periodic breathing. The model we used integrates a reduced representation of the neural controller with peripheral gas exchange and transport mechanisms. The neural controller consists of two compartments - one representing the brainstem respiratory oscillator in the pre-Bötzinger complex and another representing the rostral VRG, which transmits the rhythmic inspiratory drive to spinal motor neurons. The neural model was coupled to simplified models of the lungs incorporating oxygen and carbon dioxide transport. The model regulates both frequency and amplitude of breathing in response to partial pressures of oxygen and carbon dioxide in the blood using proportional (P) and proportional plus integral (PI) controllers, which provide chemosensory drives to the neural elements. Heart rate and heart volume are input parameters in the model.

We compared the dynamic responses of P- and PI- controllers to several stimuli. We show that a PI-controller, representing the dynamics of the neural feedback processes, fits published experimental data reported in the literature better with or without additional circulatory delay. Additional delay affected the length of apnea following the system responses to hypoxia and introduced periodic breathing in some cases. The source of the delay (blood velocity vs. distance from the lungs to chemoreceptors) is found to be important. We show that a PI-controller is associated with a shortening of the length of the ventilatory “afterdischarge” (slow recovery of ventilation) after a brief perturbation of CO2. We also show that there could be two possible mechanisms for the appearance of periodic breathing and that circulatory delay is not a necessary condition for this to happen in certain cases.
LocationWoodward 4