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Colonic Fermentation Promotes Decompression sickness in Rats.

Sébastien de Maistre1, Nicolas Vallée2, Emmanuel Gempp1

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Endogenous hydrogen production from colonic fermentation, induced by mannitol, significantly increased decompression sickness (DCS) risk in fasting rats. Inhibiting fermentation reduced DCS incidence, suggesting gut hydrogen impacts diving safety.

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Area of Science:

  • Diving physiology
  • Gastroenterology
  • Biomedical engineering

Background:

  • Decompression sickness (DCS) results from massive bubble formation after diving.
  • Hydrogen (H2) is used as an oxygen diluent in diving gases.
  • Reducing the body's H2 burden via gut microbes may mitigate DCS risk.

Purpose of the Study:

  • To investigate if colonic fermentation and endogenous hydrogen production promote DCS in fasting rats.
  • To assess the impact of mannitol-induced fermentation on DCS incidence.
  • To explore the role of gut hydrogen in diving-related pathologies.

Main Methods:

  • 93 fasting rats were divided into two groups: one force-fed mannitol, the other water, 4 hours pre-dive.
  • Exhaled hydrogen levels were measured pre- and post-force feeding.
  • Rats underwent hyperbaric exposure, and DCS incidence was recorded.
  • Metronidazole pretreatment was used to inhibit colonic fermentation in a subset of rats.

Main Results:

  • Rats fed mannitol showed a significantly higher DCS incidence (80%) compared to water-fed rats (40%).
  • Metronidazole pretreatment reduced DCS incidence in mannitol-fed rats (33%) and inhibited colonic fermentation.
  • Mannitol ingestion increased DCS in fasting rats when colonic fermentation peaked during decompression.

Conclusions:

  • Colonic fermentation leading to endogenous hydrogen production promotes DCS in fasting rats.
  • Pre-dive ingestion of substances like mannitol can exacerbate DCS risk through gut hydrogen production.
  • Findings suggest that colonic fermentation may generally promote DCS via endogenous hydrogen production, even in rats on a normal diet.