Intracoronary aqueous oxygen perfusion, performed 24 h after the onset of postinfarction reperfusion, experimentally reduces infarct size and improves left ventricular function.

Background: 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.

Aqueous oxygen near the homogeneous nucleation limit of water: stabilization with submicron capillaries.

Previous studies have demonstrated that the metastability threshold of aqueous oxygen (AO) is inversely dependent on the internal diameter of capillary tubes used to deliver it into blood. The hypothesis was tested herein that significantly higher thresholds are attainable with capillaries having markedly smaller dimensions (submicron) than those previously studied. Water was equilibrated with oxygen over a 0.

Aqueous oxygen hyperbaric reperfusion in a porcine model of myocardial infarction.

Objectives: The purpose of the study was to test the hypothesis that intracoronary aqueous oxygen (AO) hyperbaric reperfusion reduces myocardial injury after prolonged coronary occlusion. Background. Attenuation of ischemia/reperfusion injury by the use of hyperbaric oxygen (HBO) administered during reperfusion has been demonstrated for a wide variety of tissues, including myocardium.