Oku Y, Saidel G M, Cherniack N S, Altose M D
Department of Medicine, Case Western Reserve University, USA.
Med Biol Eng Comput. 1995 May;33(3):252-6. doi: 10.1007/BF02510496.
A mathematical model has been developed that includes sensations of breathlessness and a dynamic CO2 respiratory controller. Breathing sensations, which are represented as a discomfort index, are assumed to depend on arterial PCO2 level, automatic and wilful motor commands and mechanoreceptor feedback. Wilful control is assumed to arise from cortical centres of the brain and is independent of the reflex control system. The bulbopontine respiratory controller produces the automatic motor command, which is determined by chemical and mechanical feedback. Simulations demonstrate how the controller output and breathing sensations change when wilful motor commands disturb spontaneous breathing. Simulations include isocapnic hyper- and hypoventilation and deliberate hypoventilation during CO2 rebreathing. Simulations are compared with experimental data from human subjects. Simulations predict that the discomfort index intensifies when ventilation is either voluntarily raised or lowered from the optimal level; and discomfort is greater when ventilation is lowered than when it is raised at a given level of PCO2. The simulated results agree with those obtained experimentally. The simulations suggest that respiratory drive integration may depend not only on the direct effects of chemical and mechanical feedback, but also on the perceptual consequences of these stimuli.
已经开发出一种数学模型,该模型包括呼吸急促的感觉和动态二氧化碳呼吸控制器。呼吸感觉被表示为不适指数,假定其取决于动脉血二氧化碳分压水平、自动和有意的运动指令以及机械感受器反馈。有意控制被认为源于大脑的皮质中枢,并且独立于反射控制系统。延髓脑桥呼吸控制器产生自动运动指令,该指令由化学和机械反馈决定。模拟展示了当有意运动指令干扰自主呼吸时,控制器输出和呼吸感觉如何变化。模拟包括等碳酸血症时的过度通气和通气不足以及二氧化碳再呼吸期间的故意通气不足。模拟结果与来自人类受试者的实验数据进行了比较。模拟预测,当通气量从最佳水平自愿升高或降低时,不适指数会增强;并且在给定的二氧化碳分压水平下,通气量降低时的不适比升高时更大。模拟结果与实验获得的结果一致。模拟表明,呼吸驱动整合可能不仅取决于化学和机械反馈的直接作用,还取决于这些刺激的感知后果。