Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O2E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O2. Studies were carried out in 24 isolated perfused feline hearts divided into three equal groups. Groups I and II were subjected to 60 min of 37°C ischemia; Group III was protected with hypothermia (27°C) and potassium cardioplegia during the 60 min of ischemia. Group II underwent hyperosmolar (340 mOsm) reperfusion with mannitol to improve subendocardial perfusion; Groups I and III had isosmolar postischemic reperfusion. In addition to O2E determinations, myocardial O2 (PmO2) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O2E was depressed in Group I (70 ± 5% of control) and Group II (70 ± 4% of control) but was unaltered in Group III (105 ± 8% of control). This impairment of O2E was not associated with increased A-V shunting. PmO2 was not different among the three groups excluding diffusion barriers as a likely explanation. Improving transmural myocardial perfusion in Group II did not result in improvement in postischemic O2E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O2E, therefore, must be an impaired capacity for utilization of delivered O2 at the cellular level.
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