A mathematical model of CO2 effect on cardiovascular regulation

The effect of changes in arterial CO2 tension on the cardiovascular system is analyzed by means of a mathematical model. The model is an extension of a previous one that already incorporated the main reflex and local mechanis ms triggered by O-2 changes. The new aspects covered by the model are the O -2-CO2 interaction at the peripheral chemoreceptors, the effect of local CO 2 changes on peripheral resistances, the direct central neural system (CNS) response to CO2, and the control of central chemoreceptors on ventilation and tidal volume. A statistical comparison between model simulation results and various experimental data has been performed. This comparison suggests that the model is able to simulate the acute cardiovascular response to ch anges in blood gas content in a variety of conditions (normoxic hypercapnia , hypercapnia during artificial ventilation, hypocapnic hypoxia, and hyperc apnic hypoxia). The model ascribes the observed responses to the complex su perimposition of many mechanisms simultaneously working (baroreflex, periph eral chemoreflex, CNS response, lung-stretch receptors, local gas tension e ffect), which may be differently activated depending on the specific stimul us under study. However, although some experiments can be reproduced using a single basal set of parameters, reproduction of other experiments require s a different combination of the mechanism strengths (particularly, a diffe rent strength of the local CO2 mechanism on peripheral resistances and of t he CNS response to CO2). Starting from these results, some assumptions to e xplain the striking differences reported in the literature are presented. T he model may represent a valid support for the interpretation of physiologi cal data on acute cardiovascular regulation and may favor the synthesis of contradictory results into a single theoretical setting.