Levitt M D, Olsson S
Research Service, Veterans Administration Medical Center, Minneapolis, Minnesota, USA.
Gastroenterology. 1995 May;108(5):1560-5. doi: 10.1016/0016-5085(95)90707-6.
Patients with pneumatosis cystoides intestinalis have been reported to excrete excessive H2 because of a lack of H2-consuming intestinal bacteria. This study describes a patient with bacterial overgrowth and pneumatosis of the small intestine whose colonic flora avidly consumed H2 but whose small bowel flora produced but did not consume H2. There is no commonly accepted mechanism whereby excessive luminal H2 causes intramural gas. An explanation is proposed in which an initial, transitory source of intramural gas is distinguished from the mechanism that results in the persistence of the gas. Independent of the initial source of gas, rapid diffusion of H2 from the lumen into an intramural gas bubble would cause N2, O2, and CO2 to diffuse from the blood into the bubble. As a result, the bubble would expand and then persist indefinitely as long as H2 continued to diffuse from the lumen to the intramural gas collection.
据报道,患有肠壁囊样积气症的患者因缺乏消耗氢气的肠道细菌而排出过多氢气。本研究描述了一名患有小肠细菌过度生长和积气症的患者,其结肠菌群大量消耗氢气,但小肠菌群产生氢气却不消耗氢气。目前尚无普遍接受的机制来解释管腔内过量氢气如何导致肠壁内气体形成。本文提出一种解释,其中将肠壁内气体的初始短暂来源与导致气体持续存在的机制区分开来。与气体的初始来源无关,氢气从管腔快速扩散到肠壁内气泡中会导致氮气、氧气和二氧化碳从血液扩散到气泡中。结果,只要氢气继续从管腔扩散到肠壁内气体聚积处,气泡就会膨胀,然后无限期持续存在。