Intracoronary aqueous oxygen (AO) hyperoxemic perfusion, initiated shortly (15–30 min) after the onset of postinfarction reperfusion, reduces infarct size and improves left ventricular function. Whether such therapy provides similar benefits when administered many hours after the onset of reperfusion is unknown. Accordingly, the hypothesis was tested that AO hyperbaric perfusion, performed 24 h after the onset of postinfarction reperfusion, reduces infarct size and improves left ventricular ejection fraction (LVEF) in swine.

Following a 1-h balloon occlusion of the left anterior descending coronary artery in air-ventilated juvenile domestic swine, reperfusion was allowed to proceed without adjunctive therapy overnight in all animals. The following day, half of the reanesthetized, air-ventilated swine were randomized to treatment with intracoronary AO hyperbaric perfusion for 90 min (n=6, mean arterial perfusate PO₂=899±78 mm Hg), while the remainder served as controls (n=6).

Infarct size by triphenyl tetrazolium chloride was reduced by 48% and the [area of necrosis]/[area at risk] ratio was reduced by 44% in the AO group compared to the control group (p<0.05). By serial ventriculography, mean LVEF improved by 21% during AO perfusion, relative to baseline and control group values (p<0.05), with no significant change 1 h after completion of treatment (p>0.05).

AO hyperbaric perfusion, delayed 24 h after the onset of postinfarction reperfusion, reduces infarct size and improves LVEF in an experimental animal model.