Comparison of hyperbaric oxygen, ozone, and dexpanthenol therapies in rats with acute lung injury

BACKGROUND AND AIM: Acute respiratory distress syndrome (ARDS) is a fatal disease pre-senting with respiratory failure. Patients with ARDS account for a considerable portion of patients staying in the intensive care unit (ICU). Therefore, advances in the treatment of these patients are of great importance. Direct or indirect injury to the lung initiates an inflammatory process. This results in impaired integrity of the alveolar-capillary membrane, pulmonary edema, and severe hy-poxia. The present study compared hyperbaric oxygen (HBO), ozone, and dexpanthenol therapies administered to rats with experimentally induced ARDS, as well as the efficacy of these therapies. METHODS: Thirty-two male Wistar Albino rats were used in the study. The rats were divided into four groups. All groups were administered antibiotherapy for 5 days after administering live Escherichia coli. Group 1 (control group) rats received intraperitoneal saline. Group 2 rats were treated with HBO. Group 3 rats received an oxygen + ozone mixture. Group 4 rats received dex-panthenol. After 5 days, anesthesia was administered to all rats, blood gases were collected from the abdominal aorta, and then the rats were sacrificed. Some of the collected blood was used for cytokine assays. The right lung tissues were used for histopathological examination. The left lung tissues were used to measure enzyme levels. RESULTS: Histopathologically, there were intra-alveolar hemorrhage, edema, intensive inflam-matory cell infiltration, fibrosis, collapse, type 2 alveolar cells, and macrophage accumulation in all groups. In terms of fibrosis/alveolar septal thickening, the dexpanthenol group had a sig-nificantly lower mean score than the control and HBO groups. In terms of alveolar collapse, the dexpanthenol group had a significantly lower mean score than all other groups. In terms of increased macrophage and type II alveolar cell counts, the ozone group had a significantly lower mean score than all other groups. There was no significant difference in immunohistochemical staining between the groups. In terms of superoxide dismutase levels, the dexpanthenol group had a significantly lower score than the control group. Regarding IL-10 levels, the ozone group had a significantly higher score than the control and HBO groups. The dexpanthenol group had a significantly higher score only than the HBO group. Regarding PaO2 levels, the ozone group had a significantly higher score than all groups. The ozone group had a significantly lower score on PaCO2 levels than all groups. CONCLUSIONS: Among the treatments, the HBO therapy increased cell injury. The ozone therapy produced anti-inflammatory effect and histopathologically positive outcomes. The ozone therapy provided significant improvement in arterial oxygenation. The dexpanthenol therapy produced antioxidant effect and histopathologically positive outcomes. The antifibrotic effect was prominent in the dexpanthenol therapy. Further studies are needed to generalize the use of these treatments in ARDS.