The influence of hyperbaric oxygen therapy on intestinal mucosal barrier function in rats with acute carbon monoxide poisoning

Hyperbaric oxygen increases the partial pressure of O₂ in arterial blood and tissues and thereby relieves cellular hypoxia. We investigated whether this treatment changes biochemical parameters and intestinal mucosal barrier function in rats exposed to toxic levels of CO. Groups of ten Sprague–Dawley rats were treated with CO, with hyperbaric oxygen, or with CO followed by hyperbaric oxygen. A fourth group maintained under normal atmospheric conditions served as a control. CO poisoning increased red blood cell distribution width and the amount of alanine aminotransferase, urea nitrogen, and tight junction creatine kinase but decreased the mean corpuscular hemoglobin (Hb). These changes were reversed after hyperbaric oxygen therapy, which increased the number of red blood cells, hematocrit level, total protein, and Hb level. Hyperbaric oxygen therapy also increased tight junction protein 1 expression and reduced toll-like receptor 4 expression in the rat colon. In conclusion, hyperbaric oxygen resulted in an improved oxic condition in CO-poisoned rats and restored energy metabolism by repairing, to some extent, the organs injured by CO. The therapy may also improve the function of the intestinal mucosal barrier.