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Myoglobin function evaluated in working heart tissue
1Biomedical Engineering Department, Louisiana Tech University, Ruston, Louisiana 71272-0046, USA. jgardner@engr.latech.edu
Advances in Experimental Medicine and Biology
|January 16, 1999
Summary
Myoglobin does not significantly aid oxygen transport in working heart tissue. Optimized models show myoglobin diffusion is not elevated, suggesting limited facilitation of oxygen diffusion in steady-state conditions.
Area of Science:
- Physiology
- Biophysics
- Computational Biology
Background:
- Myoglobin's role in oxygen transport is debated, especially in working heart muscle.
- Previous models using literature values for myoglobin diffusion showed minimal facilitation.
- Muscle contraction may influence oxygen diffusion, potentially augmenting myoglobin's role.
Purpose of the Study:
- To investigate elevated diffusion coefficients for oxygen and myoglobin in working heart tissue.
- To model oxygen transport using the Radially-Averaged, Axially-Distributed (RAAD) model.
- To determine if myoglobin significantly facilitates oxygen diffusion in the heart.
Main Methods:
- Utilized the RAAD model, incorporating axial diffusion, myoglobin facilitation, and Michaelis-Menten oxygen consumption.
- Employed a variable-mesh finite-difference scheme for numerical solutions.
- Optimized model parameters using a Nelder-Mead simplex routine to minimize error between predicted and experimental pO2 data.
Main Results:
- Myoglobin facilitation had minimal impact on predicted oxygen distribution.
- Optimized oxygen diffusion coefficients remained elevated.
- Optimized myoglobin diffusion coefficients were lower than experimentally measured values.
Conclusions:
- Myoglobin does not significantly facilitate oxygen diffusion to tissue in the steady state.
- Myoglobin diffusion is not elevated in working heart tissue.
- Contractile mechanisms do not appear to augment myoglobin-facilitated oxygen transport in this model.