Acute respiratory distress syndrome (ARDS) features pulmonary dysfunction capable of causing life-threatening hypoxaemia. Ventilation and hyperoxic therapies force oxygen through dysfunctional alveoli but risk exacerbating damage. Ox66™ is an ingestible, solid-state oxygen product designed for oxygen supplementation. Eighteen anaesthetized, ventilated rats were subjected to a 40% reduction in tidal volume to produce a hypoventilatory simulation of the hypoxia in ARDS (HV-ARDS). After 60 min, animals were randomized to receive either normal saline (Saline; volume control) or Ox66™ gavage. Cardiovascular function and blood oximetry/chemistry were measured alongside interstitial oxygenation (PISFO2) of the peripheral spinotrapezius muscle. HV-ARDS reduced mean arterial pressure by ∼20% and PISFO2 by ∼35% for both groups. Ox66™ gavage treatment at 60 min improved PISFO2 over Saline (p < .0001), restoring baseline values, however, the effect was temporary. A second bolus at 120 min repeated the OX66™ PISFO2 response, which remained elevated over Saline (p < .01) until study end and was supported by systemic parameters of lactate, PaO2, SO2, and base deficit. Saline remained hypotensive, whereas Ox66™ became normotensive. Vasoconstriction was observed in the Saline, but not Ox66™ group. Supplemental oxygenation through Ox66™ gavage increased peripheral tissue oxygenation, warranting further study for disorders featuring dysfunction of pulmonary perfusion like ARDS.
Keywords: ARDS; COVID-19; Ox66™; microcirculation; oxygen; phosphorescence quenching microscopy.