![]() ![]() ![]() The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Ĭompeting interests: The authors have declared that no competing interests exist. All relevant data are within the paper.įunding: IAR, AB-T, and NAS are funded by grant R01NS069220 from the National Institutes of Health (NIH) ( ) JER and CP are funded by grants DMS 10217508 from the National Science Foundation ( ) YIM is funded by Indiana University - Purdue University, Indianapolis ( and JCS is funded by Intramural Research Program of the NIH, National Institute of Neurological Disorders and Stroke ( ). The work is made available under the Creative Commons CC0 public domain dedication.ĭata Availability: The authors confirm that all data underlying the findings are fully available without restriction. This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. Received: JAccepted: SeptemPublished: October 10, 2014 PLoS ONE 9(10):Įditor: Michael Koval, Emory University School of Medicine, United States of America (2014) A Closed-Loop Model of the Respiratory System: Focus on Hypercapnia and Active Expiration. The model can be used for simulation of closed-loop control of breathing under different conditions including respiratory disorders.Ĭitation: Molkov YI, Shevtsova NA, Park C, Ben-Tal A, Smith JC, Rubin JE, et al. The model suggests that the closed-loop respiratory control system switches to active expiration via a quantal acceleration of expiratory activity, when increases in breathing rate and phrenic amplitude no longer provide sufficient ventilation. The model represents the first attempt to model the transition from quiet breathing to breathing with active expiration. The lung volume is controlled by two pumps, a major one driven by the diaphragm and an additional one activated by abdominal muscles and involved in active expiration. The RTN/pFRG compartment contains an independent neural generator that is activated at an increased CO 2 level and controls the abdominal motor output. The neural component of the model simulates the respiratory network that includes several interacting respiratory neuron types within the Bötzinger and pre-Bötzinger complexes, as well as the retrotrapezoid nucleus/parafacial respiratory group (RTN/pFRG) representing the central chemoreception module targeted by chemical feedback. The lung subsystem provides two types of feedback to the neural subsystem: a mechanical one from pulmonary stretch receptors and a chemical one from central chemoreceptors. To study these mechanisms, we developed a computational model of the closed-loop respiratory system that describes the brainstem respiratory network controlling the pulmonary subsystem representing lung biomechanics and gas (O 2 and CO 2) exchange and transport. The mechanisms of this transition remain unknown. In contrast, during intense exercise or severe hypercapnia forced or active expiration occurs in which the abdominal “expiratory” muscles become actively involved in breathing. During quiet breathing, pumping air from the lungs is mostly performed by contraction of the diaphragm during inspiration, and muscle contraction during expiration does not play a significant role in ventilation. Breathing is a vital process providing the exchange of gases between the lungs and atmosphere. ![]()
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