Lack of toxic side effects in neutrophils following hyperbaric oxygen.
Undersea & hyperbaric medicine : journal of the Undersea and Hyperbaric Medical Society, Inc
confidence
Key findings
Repeated HBO2 exposure did not impair neutrophil respiratory burst or phagocytic activity, indicating no toxic effect on innate host defense.
View source on PubMed (PMID 14756233) ↗
- Sample size
- 40
- Population
- Healthy volunteers
- Dosing
- 2.5 atmospheres absolute over 90 min, single or repetitive
- Duration
- 90 min exposures; short- and long-term repetitive exposure
- Route
- Hyperbaric oxygen inhalation
- Blinding
- not_reported
- Controls
- none
- Drug class
- physical modality
Measured endpoints
- Neutrophil respiratory burst (superoxide radical production) after E. coli inductionNo changeimmunenot_significant
- Neutrophil respiratory burst after TNF-alpha priming and fMLP stimulationNo changeimmunenot_significant
- Neutrophil phagocytic activityNo changeimmunenot_significant
Full abstract
Conflicting data have been reported about the impact of repeated HBO2 exposure on the production of superoxide radicals during the neutrophil respiratory burst (RB) and on phagocytosis. In this study we wanted to see if exposure to hyperoxia would affect human neutrophil RB and phagocytosis. Short- and long-term effects after single or repetitive HBO2 exposure of 2.5 atmospheres absolute over a period of 90 min were studied in 40 healthy volunteers. The RB was measured by the intracellular oxidation of dihydrorhodamine after induction by Escherichia coli (E. coli), or priming with recombinant tumour necrosis factor alpha (TNF-alpha), followed by N-formyl-methionyl-leucyl-phenylalanine (fMLP) stimulation. The phagocytic activity was determined by the intake of FITC-labelled opsonized E. coli. No differences could be found between RB and phagocytic activity before and after HBO2 therapy, regardless of short- or long-term exposure. These findings indicate that exposure to hyperoxia does not impair these two important functions of the human innate host defense.