Background: Hypoxemia may compromise cell metabolism and organ function. Supplemental oxygen (O) at high concentrations may prove ineffective, and issues relating to hyperoxia, barotrauma, mechanical ventilation, and extracorporeal oxygenation are well documented. Old reports suggest the potential safety and efficacy of alternative routes for O administration, such as intravenous or intestinal. We re-explored these routes in rat models of hypoxemia.
Methods: Hypoxemia was induced in spontaneously breathing, anesthetized rats by breathing a hypoxic gas mix (FiO 0.1). Pilot studies infusing pure O gas caused early death, likely due to pulmonary embolism. Instead, rats (n = 6/group) were given intravenous O via a continuous infusion of pre-oxygenated Hartmann's solution (10 ml/kg/h) for 3 h with normal Ringer's lactate used in control animals. In separate experiments (n = 8/group), bowel intraluminal oxygenation was assessed with pure O administered through a cannula placed into the jejunal lumen at a dose of a 15 ml/kg bolus followed by a continuous infusion of 50 ml/kg/h; no treatment was given to controls. Echocardiography, arterial blood gas analysis, mean arterial pressure, muscle and liver tPO, muscle microvascular perfused vessel density, and urine output were measured.
Results: Administration of oxygenated Hartmann's solution (PO of solution at end-experiment = 87.5 ± 1.7 kPa) was safe but did not increase either systemic or tissue oxygenation. Similarly, the administration of bowel O was safe but did not improve neither systemic nor liver oxygenation.
Conclusions: In this rat model of hypoxemia, the intravenous infusion of gaseous O was unfeasible as it induced early mortality. Although safe, both intravenous infusion of oxygenated Hartmann's solution and bowel O administration were unable to improve arterial or tissue oxygenation.
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http://dx.doi.org/10.1186/s40635-016-0108-z | DOI Listing |
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