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1 Department of Bioengineering, University of Washington, Seattle, WA, USA
2 Department of Bioengineering, University of Washington, Seattle, WA, USA; Department of Pediatrics, University of Washington, Seattle, WA, USA; Department of Anesthesiology, University of Washington, Seattle, WA, USA
3 Department of Physiology and Biophysics, University of Washington, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: dbeard{at}bioeng.washington.ed.
An anatomically realistic model for oxygen transport in cardiac tissue is introduced for analyzing data measured from isolated perfused guinea pig hearts. The model is constructed to match the microvascular anatomy of cardiac tissue based on available morphometric data. Transport in the three-dimensional system divided into distinct microvascular, interstitial, and parenchymal spaces is simulated. The model is used to interpret experimental data on mean cardiac tissue myoglobin saturation and to reveal differences in tissue oxygenation between buffer-perfused and red cell-perfused isolated hearts. Interpretation of measured mean myoglobin saturation is strongly dependent on the oxygen content of the perfusate (e.g., red cell-containing versus cell-free). Model calculations match experimental values of mean tissue myoglobin saturation, measured mean myoglobin, and venous oxygen tension, and can be used to predict distributions of intracellular oxygen tension. Calculations reveal that approximately 20% of the tissue is hypoxic with an oxygen tension of less than 0.5 mmHg when the buffer is equilibrated with 95% oxygen to give an arterial oxygen tension of over 600 mmHg. The addition of red cells to give a hematocrit of only 5% prevents tissue hypoxia. It is incorrect to assume that the usual buffer-perfused Langendorff heart preparation is adequately oxygenated for flows in the range of 10 ml min-1 or less per ml of tissue.
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