Mathematical evidence for flow-induced changes in myocardial oxygen consumption.

Abstract

The objective of this investigation was to aid in the determination of the mechanism by which oxygen consumption changes in proportion to coronary perfusion pressure or coronary blood flow. A mathematical model of oxygen transport and consumption in the isolated-perfused heart was developed, based on data from an autoregulating, cell-free perfused, externally paced, isovolumic feline heart preparation. The model features the unique combination of Michaelis-Menten kinetics, and one-dimensional (axial) diffusion in radially well-mixed tissue. An adaptive finite-difference integration routine was used to solve the resulting third order stiff two-point boundary value problem. A simplex minimization was employed to determine the parameter values that minimized the squared difference between the model and the experimental data in terms of tissue PO2 distribution (histograms). Different cases of the model representing pressure-induced, flow-induced, and "magnified" flow effects were run. The flow-dependent oxygen consumption version of the model produced a histogram squared error 30% lower than the pressure-induced version and 5% lower than any other case. The model and a critical review of the literature indicate that a flow-related mechanism is responsible for this phenomenon. Evidence also demonstrates that the Michaelis-Menten kinetics constant is not constant for different oxygen tensions.