Mechanism of defective oxygen extraction following global ischemia

Abstract Prolonged global ischemia has been shown to result in a defect in oxygen extraction (O 2 E) which is not related to postischemic changes in coronary blood flow or ventricular contractility. Possible explanations for this defect include either (1) decreased O 2 delivery due to diffusion barriers, arterial-venous (A-V) shunting, or myocardial flow maldistribution, or (2) an impaired cellular ability to utilize delivered O 2 . 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 O 2 E determinations, myocardial O 2 ( P m O 2 ) was monitored continuously by mass spectrometry. Radioactive microspheres were used to measure both A-V shunting and endo/epi flow ratios. Postischemic O 2 E 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 O 2 E was not associated with increased A-V shunting. P m O 2 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 O 2 E making flow maldistribution an unlikely cause of this defect. The mechanism of defective postischemic O 2 E, therefore, must be an impaired capacity for utilization of delivered O 2 at the cellular level.