ArticleScientific reports2018
Stimulating fermentation by the prolonged acceleration of gut transit protects against decompression sickness.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- COInternational journal of environmental research and public health · 2024Article
- Comparison of gut microbiota immunity and pathology in specific-pathogen-free chickens with glandular and muscular gastritis using different methods.Frontiers in veterinary science · 2024Article
- Imbalance of Microbacterial Diversity Is Associated with Functional Prognosis of Stroke.Neural plasticity · 2023Article
- Highlighting of the interactions of MYD88 and NFKB1 SNPs in rats resistant to decompression sickness: toward an autoimmune response.Frontiers in physiology · 2023Article
- Cecal Metabolomic Fingerprint of Unscathed Rats: Does It Reflect the Good Response to a Provocative Decompression?Frontiers in physiology · 2022Article
- Evidence of a hormonal reshuffle in the cecal metabolome fingerprint of a strain of rats resistant to decompression sickness.Scientific reports · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Massive bubble formation after diving can lead to decompression sickness (DCS). Gut fermentation at the time of a dive exacerbates DCS due to endogenous hydrogen production. We sought to investigate whether medium-term stimulation of fermentation as a result of polyethylene glycol (PEG)-induced acceleration of bowel transit before diving exacerbates DCS in rats. Seven days before an experimental dry dive, 60 rats were randomly divided in two groups: an experimental group treated with PEG (n = 30) and an untreated control group (n = 30). Exhaled hydrogen was measured before the dive. Following hyperbaric exposure, we assessed for signs of DCS. After anaesthetisation, arterial blood was drawn to assay inflammatory cytokines and markers of oxidative stress. PEG led to a significant increase in exhaled H
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