Hyperbaric oxygen ameliorates worsening signs and symptoms of post-traumatic stress disorder

Hyperbaric oxygen therapy at 2.4 atmospheric pressure absolutes for 90 minutes per day ameliorated the signs and symptoms of agitation, confusion, and emotional distress in a 27-year-old male seven days following a traumatic accident. Hyperbaric oxygen was used to treat the patient’s crush injury and underlying nondisplaced pelvic fractures which were sustained in a bicycle versus automobile traffic accident. Its effect on the patient’s neuropsychiatric symptoms was surprising and obvious immediately following the initial hyperbaric oxygen treatment. Complete cognitive and psychiatric recovery was achieved by the seventh and final hyperbaric oxygen treatment. We propose that hyperbaric oxygen was effective in improving the patient’s neuropsychiatric symptoms by reducing cerebral oxidative stress, inflammation, vasogenic edema, and hippocampal neuronal apoptosis. Further investigation into the use of hyperbaric oxygen as a novel therapy for the secondary prevention of post-traumatic stress disorder that often accompanies post-concussive syndrome may be warranted. We acknowledge that hyperbaric oxygen therapy has been shown to have a strong placebo effect on neurologic and psychiatric diseases

Hyperbaric Oxygen Therapy Alters Vascular Reactivity Independent of Elevations in ATP

Hyperbaric oxygen (HBO) is a pharmacologic therapy used treat a variety of medical conditions. The underlying mechanisms of HBOs effect on vascular reactivity are poorly understood. The purpose of this study was to record the acute effects of HBO on vascular reactivity and determine the potential role of ATP in mediating these effects. Porcine mesenteric arteries were dissected and mounted in isolated organ baths to record changes in tension in response to potassium chloride (KCl, 15-60 mM), phenylephrine (PHE, 10-7-10-4 M), and sodium nitroprusside (SNP, 10-7-10-4 M) following a 2-hour exposure to HBO (1.75 ATA). HBO augmented responses to KCl and PHE compared to control arteries exposed to room air or nitrogen at 1.75 ATA as well as to room air at 1 atm. When compared to the 1 ATA room air control, KCl-induced constriction was significantly increased for the HBO exposure. Treatment with HBO also augmented vascular responses to PHE and SNP relative to nitrogen, but not ambient air. We hypothesized that HBO increased ATP production in vascular smooth muscle leading to enhanced vascular reactivity. Consequently, ATP levels were measured in mesenteric arteries but no significant differences in ATP levels were observed regardless of hyperbaric treatment. Direct measurements of ATPs’ effects on porcine vasculature with and without hyperbaric treatment resulted in no significant findings. These results suggest that HBO alters vascular reactivity independent of elevations in ATP