THERAPEUTIC HYPEROXIA DIMINISHES MYOCARDIAL STUNNING

We used a model of isolated coronary perfusion to answer the question: Does high PO2 during low flow myocardial ischemia diminish postischem ic myocardial contractile dysfunction? In 12 anesthetized, open chest swine, the left anterior descending (LAD) coronary artery was cannulat ed and perfused via an extracorporeal circuit. Normoxic arterial blood was pumped through a pediatric membrane oxygenator, which was used to control arterial PO2 in the perfusion bed. Myocardial stunning was cr eated by reducing LAD coronary artery flow to 40% of control values fo r 30 minutes. After 5 minutes of ischemia, swine were randomized to ei ther continued coronary normoxia or to coronary hyperoxia. In the hype roxic group, oxygen was substituted for nitrogen in the oxygenator, th us increasing coronary PO2 to 382 +/- 32 mmHg. After 30 minutes of isc hemia, all swine were reperfused with normoxic blood. Results: There w ere no significant baseline differences between the two groups with re gard to baseline hemodynamics, myocardial blood flow, or oxygen delive ry parameters. Preischemic systolic shortening was comparable in the n ormoxic and hyperoxic groups: 23.6 +/- 6.8% and 24.9 +/- 3.9%, respect ively. Increasing coronary arterial PO2 to 382 mmHg during ischemia le d to a significant decrease in myocardial stunning in the hyperoxic gr oup. Post-ischemic systolic shortening in the hyperoxic treatment grou p, 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 PO2, when used as a trea tment during transient myocardial ischemia, can diminish postischemic myocardial stunning substantially.