de Maistre Sébastien, Vallee Nicolas, Gempp Emmanuel, Louge Pierre, Duchamp Claude, Blatteau Jean-Eric
Service de Médecine Hyperbare et Expertise Plongée, Hôpital d'Instruction des Armées Sainte-Anne, Toulon, France;
Équipe Résidente de Recherche Subaquatique Opérationnelle, Institut de Recherche Biomédicale des Armées, Toulon, France; and.
J Appl Physiol (1985). 2016 Oct 1;121(4):973-979. doi: 10.1152/japplphysiol.00503.2016. Epub 2016 Sep 15.
Massive bubble formation after diving can lead to decompression sickness (DCS) that can result in neurological disorders. In experimental dives using hydrogen as the diluent gas, decreasing the body's H burden by inoculating hydrogen-metabolizing microbes into the gut reduces the risk of DCS. In contrast, we have shown that gut bacterial fermentation in rats on a standard diet promotes DCS through endogenous hydrogen production. Therefore, we set out to test these experimental results in humans. Thirty-nine divers admitted into our hyperbaric center with neurological DCS (Affected Divers) were compared with 39 healthy divers (Unaffected Divers). Their last meal time and composition were recorded. Gut fermentation rate was estimated by measuring breath hydrogen 1-4 h after the dive. Breath hydrogen concentrations were significantly higher in Affected Divers (15 ppm [6-23] vs. 7 ppm [3-12]; P = 0.0078). With the use of a threshold value of 16.5 ppm, specificity was 87% [95% confidence interval (CI) 73-95] for association with neurological DCS onset. We observed a strong association between hydrogen values above this threshold and an accident occurrence (odds ratio = 5.3, 95% CI 1.8-15.7, P = 0.0025). However, high fermentation potential foodstuffs consumption was not different between Affected and Unaffected Divers. Gut fermentation rate at dive time seemed to be higher in Affected Divers. Hydrogen generated by fermentation diffuses throughout the body and could increase DCS risk. Prevention could be helped by excluding divers who are showing a high fermentation rate, by eliminating gas produced in gut, or even by modifying intestinal microbiota to reduce fermentation rate during a dive.
潜水后大量气泡形成可导致减压病（DCS），进而引发神经紊乱。在以氢气作为稀释气体的实验潜水中，通过向肠道接种氢代谢微生物来减轻身体的氢负荷可降低减压病风险。相比之下，我们已经表明，标准饮食的大鼠肠道细菌发酵通过内源性产氢促进减压病。因此，我们着手在人体中验证这些实验结果。将39名因神经型减压病入住我们高压氧治疗中心的潜水员（患病潜水员）与39名健康潜水员（未患病潜水员）进行比较。记录他们最后一餐的时间和食物组成。通过测量潜水后1 - 4小时的呼出气氢气来估算肠道发酵速率。患病潜水员的呼出气氢气浓度显著更高（15 ppm [6 - 23] 对比 7 ppm [3 - 12]；P = 0.0078）。使用16.5 ppm的阈值时，与神经型减压病发病相关的特异性为87% [95%置信区间（CI）73 - 95]。我们观察到高于此阈值的氢气值与事故发生之间存在强烈关联（优势比 = 5.3，95% CI 1.8 - 15.7，P = 0.0025）。然而，患病潜水员和未患病潜水员在高发酵潜力食物的摄入量上并无差异。患病潜水员潜水时的肠道发酵速率似乎更高。发酵产生的氢气会扩散至全身，可能增加减压病风险。排除发酵速率高的潜水员、消除肠道产生的气体，甚至通过改变肠道微生物群来降低潜水期间的发酵速率，可能有助于预防减压病。
