Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress
Acute respiratory distress syndrome (ARDS) is a complication of pulmonary disease that produces life-threatening hypoxaemia. Despite ventilation and hyperoxic therapies, undetected hypoxia can manifest in capillary beds leading to multi-organ failure. Ox66™ is an ingestible, solid-state form of oxyg...
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Taylor & Francis Group
2024-12-01
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| Series: | Artificial Cells, Nanomedicine, and Biotechnology |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/21691401.2024.2307462 |
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| author | Bjorn K. Song Danuel A. Carr Erica D. Bruce William H. Nugent |
| author_facet | Bjorn K. Song Danuel A. Carr Erica D. Bruce William H. Nugent |
| author_sort | Bjorn K. Song |
| collection | DOAJ |
| description | Acute respiratory distress syndrome (ARDS) is a complication of pulmonary disease that produces life-threatening hypoxaemia. Despite ventilation and hyperoxic therapies, undetected hypoxia can manifest in capillary beds leading to multi-organ failure. Ox66™ is an ingestible, solid-state form of oxygen designed to supplement oxygen deficits. Twenty-four anaesthetized rats underwent a two-hit model of respiratory distress (ARDS), where a single dose (5 mg/kg) of lipopolysaccharide (LPS) was given intratracheally, and then the respiratory tidal volume was reduced by 40%. After 60 min, animals were randomized to receive Ox66™, or normal saline (NS; vehicle control) via gavage or supplemental inspired oxygen (40% FiO2). A second gavage was administered at 120 min. Cardiovascular function and blood oximetry/chemistry were measured alongside the peripheral spinotrapezius muscle’s interstitial oxygenation (PISFO2). ARDS reduced mean arterial pressure (MAP) and PISFO2 compared to baseline (BL) for all treatment groups. Treatment with Ox66 or NS did not improve MAP, but 40% FiO2 caused a rapid return to BL. PISFO2 improved after treatment with Ox66™ and 40% FiO2 and remained elevated for both groups against NS until study conclusion. Both oxygen treatments also suppressed the inflammatory response to LPS, suggesting that Ox66™ can deliver therapeutically-impactful levels of oxygen in situations of pulmonary dysfunction. |
| format | Article |
| id | doaj-art-852d64c0c2f943f0b265bca11a9cc58d |
| institution | Kabale University |
| issn | 2169-1401 2169-141X |
| language | English |
| publishDate | 2024-12-01 |
| publisher | Taylor & Francis Group |
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| series | Artificial Cells, Nanomedicine, and Biotechnology |
| spelling | doaj-art-852d64c0c2f943f0b265bca11a9cc58d2024-12-06T10:48:00ZengTaylor & Francis GroupArtificial Cells, Nanomedicine, and Biotechnology2169-14012169-141X2024-12-0152111412110.1080/21691401.2024.2307462Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distressBjorn K. Song0Danuel A. Carr1Erica D. Bruce2William H. Nugent3Song Biotechnologies LLC, Baltimore, MD, USASong Biotechnologies LLC, Baltimore, MD, USADepartment of Environmental Science, Baylor University, Waco, TX, USASong Biotechnologies LLC, Baltimore, MD, USAAcute respiratory distress syndrome (ARDS) is a complication of pulmonary disease that produces life-threatening hypoxaemia. Despite ventilation and hyperoxic therapies, undetected hypoxia can manifest in capillary beds leading to multi-organ failure. Ox66™ is an ingestible, solid-state form of oxygen designed to supplement oxygen deficits. Twenty-four anaesthetized rats underwent a two-hit model of respiratory distress (ARDS), where a single dose (5 mg/kg) of lipopolysaccharide (LPS) was given intratracheally, and then the respiratory tidal volume was reduced by 40%. After 60 min, animals were randomized to receive Ox66™, or normal saline (NS; vehicle control) via gavage or supplemental inspired oxygen (40% FiO2). A second gavage was administered at 120 min. Cardiovascular function and blood oximetry/chemistry were measured alongside the peripheral spinotrapezius muscle’s interstitial oxygenation (PISFO2). ARDS reduced mean arterial pressure (MAP) and PISFO2 compared to baseline (BL) for all treatment groups. Treatment with Ox66 or NS did not improve MAP, but 40% FiO2 caused a rapid return to BL. PISFO2 improved after treatment with Ox66™ and 40% FiO2 and remained elevated for both groups against NS until study conclusion. Both oxygen treatments also suppressed the inflammatory response to LPS, suggesting that Ox66™ can deliver therapeutically-impactful levels of oxygen in situations of pulmonary dysfunction.https://www.tandfonline.com/doi/10.1080/21691401.2024.2307462ARDSOx66phosphorescencequenchingmicroscopyoxygen |
| spellingShingle | Bjorn K. Song Danuel A. Carr Erica D. Bruce William H. Nugent Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress Artificial Cells, Nanomedicine, and Biotechnology ARDS Ox66 phosphorescence quenching microscopy oxygen |
| title | Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress |
| title_full | Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress |
| title_fullStr | Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress |
| title_full_unstemmed | Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress |
| title_short | Oxygenation through oral Ox66 in a two-hit rodent model of respiratory distress |
| title_sort | oxygenation through oral ox66 in a two hit rodent model of respiratory distress |
| topic | ARDS Ox66 phosphorescence quenching microscopy oxygen |
| url | https://www.tandfonline.com/doi/10.1080/21691401.2024.2307462 |
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