Yamamoto W S
Am J Physiol. 1980 Jan;238(1):R28-35. doi: 10.1152/ajpregu.1980.238.1.R28.
A mathematical model portraying a humoral signal derived from time-dependent variations in arterial carbon dioxide tension (PaCO2) and a neural signal proportional to the metabolic CO2 production was tested by computer simulation. The signals were assumed to enter the central mechanism through afferent pathways connected in reciprocal inhibition. The central mechanism, previously described, contained proportional, gradient, and positive feedback components. The model simulates steady-state isocapnic hyperpnea under endogenous CO2 load and hyperpnea proportional to PaCO2 under exogenous CO2 load. This behavior is consistent whether the neural signal is present alone, the humoral signal is present alone, or both are present and synergistic. When the neural and humoral signals are opposed hypocapnia and hyperventilation ensue; the values being consistent with the isometabolic hyperbola. The model also portrays steady-state behavior when CO2 is inhaled during exercise. During hypometabolic states of rest the mechanism appears to become insensitive to PaCO2 levels.
通过计算机模拟测试了一个数学模型，该模型描绘了源自动脉二氧化碳分压（PaCO2）随时间变化的体液信号以及与代谢性二氧化碳产生成正比的神经信号。假定这些信号通过相互抑制连接的传入通路进入中枢机制。先前描述的中枢机制包含比例、梯度和正反馈成分。该模型模拟了内源性二氧化碳负荷下的稳态等碳酸血症性通气过度以及外源性二氧化碳负荷下与PaCO2成正比的通气过度。无论神经信号单独存在、体液信号单独存在，还是两者都存在且具有协同作用，这种行为都是一致的。当神经信号和体液信号相互对抗时，会出现低碳酸血症和通气过度；这些值与等代谢双曲线一致。该模型还描绘了运动期间吸入二氧化碳时的稳态行为。在静息的低代谢状态下，该机制似乎对PaCO2水平变得不敏感。
