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Colonic Fermentation Promotes Decompression sickness in Rats

机译:结肠发酵促进大鼠的减压疾病

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Massive bubble formation after diving can lead to decompression sickness (DCS). During dives with hydrogen as a diluent for oxygen, decreasing the body's H2 burden by inoculating hydrogen-metabolizing microbes into the gut reduces the risk of DCS. So we set out to investigate if colonic fermentation leading to endogenous hydrogen production promotes DCS in fasting rats. Four hours before an experimental dive, 93 fasting rats were force-fed, half of them with mannitol and the other half with water. Exhaled hydrogen was measured before and after force-feeding. Following the hyperbaric exposure, we looked for signs of DCS. A higher incidence of DCS was found in rats force-fed with mannitol than in those force-fed with water (80%, [95%CI 56, 94] versus 40%, [95%CI 19, 64], p??0.01). In rats force-fed with mannitol, metronidazole pretreatment reduced the incidence of DCS (33%, [95%CI 15, 57], p?=?0.005) at the same time as it inhibited colonic fermentation (14?±?35?ppm versus 118?±?90?ppm, p?=?0.0001). Pre-diveingestion of mannitol increased the incidence of DCS in fasting rats when colonic fermentation peaked during the decompression phase. More generally, colonic fermentation in rats on a normal diet could promote DCS through endogenous hydrogen production.
机译:潜水后的巨大泡沫形成可导致减压疾病(DCS)。在耐氢作为稀释剂的渗透期间,通过将氢代谢微生物接种到肠道中降低了身体的H2负荷来降低DCS的风险。因此,我们开始研究是否导致内源性氢气产生的结肠发酵促进了禁食大鼠中的DC。在实验潜水前四个小时,93只紧固大鼠喂养,其中一半用甘露醇,另一半用水。在饲喂喂养之前和之后测量呼出的氢。在高压曝光之后,我们寻找DCS的迹象。在用甘露醇喂养的大鼠中发现DCs的较高发病率比用水进料(80%,[95%CI 56,94]与40%,[95%CI 19,64],p≤ZΩ ?0.01)。在用甘露醇抑制结肠发酵的同时,在用甘露醇喂养甘露醇的大鼠中,甲硝唑预处理降低了DCS的发生率(33%,[95%,[95%,[95%CI 15,57],p?= 0.005)(14?±35? ppm与118?±90?ppm,p?= 0.0001)。甘露醇的预滴度增加了在减压阶段达到峰值的结肠发酵时DCS在空腹大鼠中的发生率。更一般地,正常饮食大鼠的结肠发酵可以通过内源性氢气产生促进DC。

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