Therapeutic Hyperoxia Diminishes Myocardial Stunning

We used a model of isolated coronary perfusion to answer the question: Does high PO 2 during low flow myocardial ischemia diminish postischemic myocardial contractile dysfunction? In 12 anesthetized, open chest swine, the left anterior descending (LAD) coronary artery was cannulated and perfused via an extracorporeal circuit. Normoxic arterial blood was pumped through a pediatric membrane oxygenator, which was used to control arterial PO 2 in the perfusion bed. Myocardial stunning was created by reducing LAD coronary artery flow to 40% of control values for 30 minutes. After 5 minutes of ischemia, swine were randomized to either continued coronary normoxia or to coronary hyperoxia. In the hyperoxic group, oxygen was substituted for nitrogen in the oxygenator, thus increasing coronary PO 2 to 382 ± 32 mmHg. After 30 minutes of ischemia, all swine were reperfused with normoxic blood. Results: There were no significant baseline differences between the two groups with regard to baseline hemodynamics, myocardial blood flow, or oxygen delivery parameters. Preischemic systolic shortening was comparable in the normoxic and hyperoxic groups: 23.6 ± 6.8% and 24.9 ± 3.9%, respectively. Increasing coronary arterial PO 2 to 382 mmHg during ischemia led to a significant decrease in myocardial stunning in the hyperoxic group. Post‐ischemic systolic shortening in the hyperoxic treatment group, measured at 15, 30, 45, and 60 minutes of reperfusion, was 14.8% ± 6.3% (p < 0.05), 13.4% ± 6.4% (p < 0.05), 13.8% ± 6.7% (p < 0.05), and 14.3% ± 5.8% (p < 0.05) compared to comparable measurements in the normoxic control group of 9.0% ± 5.4%, 7.8% ± 5.0%, 7.8% ± 5.2%, and 7.2% ± 5.1%. We conclude that high PO 2 , when used as a treatment during transient myocardial ischemia, can diminish postischemic myocardial stunning substantially.