A new computational model is developed to characterize the dynamical aspects of simultaneous blood‐tissue transport and exchange of O2, CO2, HCO3− and H+ in the coronary microcirculation by accurately simulating the rapidly changing intra‐capillary concentration profiles as the blood gets warmed, acidified, deoxygenated, and carbonated while flowing through the myocardial capillaries. It is based on our 2006 steady‐state, nonlinear, convection‐diffusion‐permeation‐reaction computational model of circulating blood gases, hemoglobin (Hb) binding, and acid‐base buffering in the blood which is available for download from our JSim model repository (http://www.physiome.org/jsim/models/webmodel/NSR/Exchange_O2_CO2_HCO3_and_H+). The kinetics are complicated by: (i) intravascular axial diffusion, (ii) RBC/plasma velocity ratio > 1, (iii) gas and ion permeation through RBC, endothelial and cell membranes, (iv) carbonic anhydrase‐catalyzed CO2 hydration reaction and HCO3‐ buffering in blood and tissue, (v) nonlinear competitive temperature‐dependent binding of Hb, O2, CO2 and H+ inside RBCs, (vi) myoglobin‐facilitated transport of O2 in cardiac cells, and (vii) O2 consumption and CO2 production inside mitochondria, with CO2 production and the respiratory quotient dependent upon the substrates, gas concentrations, cardiac work levels, and the rate of mitochondrial oxidative phosphorylation. These interactions smooth the axial spatial gradations in fluxes of O2 from blood into tissue and of CO2 out into the lung air. The simplest version of this extended model focuses on intracapillary RBC‐plasma interactions and the conditions for alveolar‐arterial differences in oxygen saturation. The cell‐tissue versions incorporate a new kinetic model of cytochrome c oxidase (CcO) that accurately characterizes the kinetics of O2 consumption by CcO as a function of cytochrome c redox fraction, mitochondrial inner membrane electrical and proton gradients (i.e. proton motive force; energy state), O2, and pH. The model serves as the dynamical exchange component of whole body gas exchange and acid‐base regulation. With augmentation to bind 15O2 or 17O2, this model can be used for the analysis of dynamic PET image sequences or NMR studies for estimating the regional tissue O2 consumption.Support or Funding InformationSupported by NIH grant U01‐HL122199
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