Limitations of tracer oxygen uptake in the canine coronary circulation

Theoretical models of oxygen transport in the myocardium have failed to account for low average tissue pO2 relative to to coronary sinus pO2, measured with pO2 electrodes and myoglobin saturation, and for hypoxic contractile failure at relatively high coronary sinus pO2 levels. These findings could be explained by either arteriovenous diffusional shunting or a limiting rate of transfer of oxygen from blood to tissue, or both. To gain new insights, we performed multiple indicator dilution tracer experiments across the coronary circulation in the dog, with 18O2 as the oxygen tracer and 51Cr-labeled red cells as the reference tracer for oxygen. 125I-Albumin and 22Na+ were included to provide the relative plasma flow rate. The tracer oxygen outflow curve consisted of a large early peak related to its reference red cell curve. No tracer emerged before the labeled red cells. The downslope, which contains the returning component of the tracer curve, decreased less steeply when oxygen consumption was reduced by propranolol. Fitting the tracer oxygen outflow curve with a distributed model including irreversible sequestration behind a resistance gave a transfer rate constant which was relatively small, and a relatively large rate constant for sequestration. Relative oxygen consumption (estimated from the arteriovenous difference) correlated closely with the rate constant for sequestration. Estimated average tissue oxygen concentrations were of the order of one-third blood concentration. Dimensional analysis indicates that the low transfer rate constant derives from hemoglobin-oxygen binding; this decreases fractional tracer oxygen transfer in proportion to the ratio of plasma:red cell oxygen pools.