Aqueous Oxygen

Abstract

Background High levels of hyperoxemia may have utility in the treatment of regional tissue ischemia, but current methods for its implementation are impractical. A catheter-based method for infusion of O 2 , dissolved in a crystalloid solution at extremely high concentrations, ie, 1 to 3 mL O 2 /g (aqueous oxygen [AO]), into blood without bubble nucleation was recently developed for the potential hyperoxemic treatment of regional tissue ischemia. Methods and Results To test the hypotheses that hypoxemia is correctable and that hyperoxemia can be produced locally by AO infusion, normal saline equilibrated with O 2 at 3 MPa (30 bar; 1 mL O 2 /g) was delivered into arterial blood in two different animal models. In 15 New Zealand White rabbits with systemic hypoxemia, AO was infused into the midabdominal aorta at 1 g/min. Mean distal arterial P o 2 increased to 236±113 and 593±114 mm Hg on 1-hour periods of air and O 2 breathing, respectively, from a baseline of 70±10 mm Hg ( P <.01). In contrast, infusion of ordinary normal saline in a control group (n=7) had no effect on arterial P o 2 . No differences between groups ( P >.05) in temporal changes in blood counts and chemistries were identified. In 10 dogs, low coronary blood flow in the circumflex artery was delivered with a roller pump through the central channel of an occluding balloon catheter. Hypoxemic, normoxemic, and AO-induced hyperoxemic blood perfusates (mean P o 2 , 52±4, 111±22, and 504±72 mm Hg, respectively) were infused for 3-minute periods in a randomized sequence. Short-axis two-dimensional echocardiography demonstrated a significant decrease ( P <.05) in left ventricular ejection fraction compared with baseline physiological values with low-flow hypoxemic and normoxemic perfusion but not with low-flow hyperoxemic perfusion. Conclusions Intra-arterial AO infusion was effective in these models for regional correction of hypoxemia and production of hyperoxemia.