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Analytical solutions to the model problem of unsteady Newtonian fluid flow in straight, elastic-walled vessels can provide: theoretical insights into the flow of blood in arteries; a theoretical basis for clinical measurements in diagnoses of arterial flow rates; and guidance for boundary conditions in numerical simulations of flow in finite computational domains. However, while Womersley's analyses of blood flow assume solution forms that treat the flow as periodic and continuously unsteady, many flow variables in the smaller arteries are not continuously unsteady at all. They are characterized more accurately as rapid transient motions followed by a period of recovery to a stationary state, repeated in successive cycles. These flows are not continually unsteady ones described by Womersley's solutions but unsteady flows restarted from rest in each cycle, characterized as initial-boundary value problems. In this paper, we compare the Womersley and initial-boundary value solutions for model transients that stop then restart, explain these previously unreported limitations of Womersley's solutions, and demonstrate how the initial-boundary value solutions provide excellent agreement with measurements of blood flow in the anterior tibial and popliteal arteries of patients. Some consequences of these findings for understanding and interpreting measurements of blood flow, and for prescribing boundary conditions in computer simulations of arterial blood flow are discussed., (© 2011 – IOS Press and the authors. All rights reserved)

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., Methods: 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 PO(2)=899+/-78 mm Hg), while the remainder served as controls (n=6)., Results: 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)., Conclusion: AO hyperbaric perfusion, delayed 24 h after the onset of postinfarction reperfusion, reduces infarct size and improves LVEF in an experimental animal model.

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 0.3- to 0.7-k bar range. Inert gases (argon, helium) facilitated studies at pressures to 2.5 k bar. An argon-ion laser was used to visualize fluorescein in the liquid effluent from silica capillaries that were tapered at the distal end to a submicron internal diameter (0.5 +/- 0.3 microns). During infusion of the fluorescent effluent into host water at 21 degrees C and atmospheric pressure, integrity of the effluent and lack of microbubbles were monitored by videomicroscopy. No microbubbles were noted at AO concentrations ranging from 7.5 to 12.8 ml O2/g (0.34 to 0.68 k bar, respectively) or in the aqueous argon effluent at concentrations to 14 ml Ar/g (0.75 k bar). For aqueous helium, effluent nucleation was not observed at a mean concentration of 13 +/- 3 ml He/g (2.0 +/- 0.5 k bar), with an upper value of 15.2 ml He/g (2.4 k bar). The data represent the highest values of the tensile strength of water ever observed and approximate its theoretical homogeneous nucleation limit. Thus, remarkably high metastable concentrations of AO and other gases are attainable with the use of submicron capillaries.

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. We have recently developed a more practical, catheter-based, site-specific method for delivery of oxygen at hyperbaric levels with aqueous oxygen infusion., Methods: Following a 60-minute balloon occlusion of the left anterior descending coronary artery in swine, intracoronary AO hyperoxemic perfusion (50 mL blood/minute; 1.5 mL AO/minute; mean pO2 = 834 104 mmHg) was performed for 90 minutes after a 15-minute period of normoxemic autoreperfusion (physiologic reperfusion). Control groups consisted of autoreperfusion alone; active normoxemic perfusion (50 mL/minute) for 90 minutes; and hyperoxemic perfusion with a hollow fiber oxygenator (HFO) for 90 minutes. Results. A significant improvement in left ventricular ejection fraction was noted by ventriculography at 105 minutes of reperfusion (ANOVA, p < 0.05), compared to the 15-minute autoreperfusion period, only in the AO and HFO groups. Mean percent infarct size (area of necrosis)/(area at risk), quantitative post-mortem hemorrhage score, and myocardial myeloperoxidase levels at 3 hours of reperfusion were significantly less in the AO group (ANOVA, p < 0.05), but not in the HFO group, compared to normoxemic groups. Conclusions. The results demonstrate that intracoronary hyperbaric reperfusion with AO, but not with a membrane oxygenator, attenuates myocardial ischemia/reperfusion injury.

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 O2, dissolved in a crystalloid solution at extremely high concentrations, ie, 1 to 3 mL O2/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 O2 at 3 MPa (30 bar; 1 mL O2/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 PO2 increased to 236+/-113 and 593+/-114 mm Hg on 1-hour periods of air and O2 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 PO2. 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 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 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.