A HIGHLY O-2-SUPERSATURATED INFUSATE FOR REGIONAL CORRECTION OF HYPOXEMIA AND PRODUCTION OF HYPEROXEMIA

Background High levels of hyperoxemia may have utility in the treatmen t of regional tissue ischemia, but current methods for its implementat ion are impractical. A catheter-based method for infusion of O-2, diss olved in a crystalloid solution at extremely high concentrations, ie, 1 to 3 mL O-2/g (aqueous oxygen [AO]), into blood without bubble nucle ation was recently developed for the potential hyperoxemic treatment o f regional tissue ischemia. Methods and Results To test the hypotheses that hypoxemia is correctable and that hyperoxemia can be produced lo cally 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 a nimal models. In 15 New Zealand White rabbits with systemic hypoxemia, AO was infused into the midabdominal aorta at 1 g/min. Mean distal ar terial PO2 increased to 236+/-113 and 593+/-114 mm Hg on 1-hour period s of air and O-2 breathing, respectively, from a baseline of 70+/-10 m m Hg (P<.01). In contrast, infusion of ordinary normal saline in a con trol group (n=7) had no effect on arterial PO2. No differences between groups (P>.05) in temporal changes in blood counts and chemistries we re identified. In 10 dogs, low coronary blood flow in the circumflex a rtery was delivered with a roller pump through the central channel of an occluding balloon catheter. Hypoxemic, normoxemic, and AO-induced h yperoxemic blood perfusates (mean PO2, 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 com pared with baseline physiological values with low-flow hypoxemic and n ormoxemic perfusion but not with low-flow hyperoxemic perfusion. Concl usions Intra-arterial AO infusion was effective in these models for re gional correction of hypoxemia and production of hyperoxemia.