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在十二指肠溃疡粘膜活性氧代谢产物生产。
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  1. G R戴维斯,
  2. N J·西蒙斯,
  3. T R史蒂文斯,
  4. 一个Grandison,
  5. D R布莱克,
  6. D S。兰普顿
  1. 部门组织病理学,伦敦医院医学院,伦敦。

    文摘

    研究假设活性氧代谢产物是重要的病理生理学的十二指肠溃疡疾病,其生产的十二指肠粘膜活检标本测量使用鲁米诺和lucigenin放大化学发光。鲁米诺化学发光,表示为背景修正平均光子发射/毫克/分钟x 10(3)(95%置信区间),在十二指肠炎症增加评估宏观上:溃疡20.3 (4.8 - 51.3),n = 29;严重十二指肠炎13.9 (6.6 - 75.3),n = 16;轻微的十二指肠炎0.0 (-0.5 - 0.8),n = 56;控制-0.8 (-1.3 - -0.1),n = 41;p = 0.0001,克鲁斯卡尔-沃利斯)和镜下:严重17.0 (9.3 - 51.3),n = 12;温和的0.3 (-2.8 - 5.8),n = 17;轻微的-0.1 (-1.8 - 1.0),n = 17;控制-0.8 (-1.6 - 0.0),n = 15;(p = 0.0001)。 Luminol chemiluminescence was directly related to both the macroscopic and microscopic severity of duodenal damage (Spearman's R = + 0.53, + 0.55 respectively, both p = 0.0001), to histochemical assessment (myeloperoxidase activity) of neutrophil infiltration (R = + 0.63; p = 0.04), and to lucigenin chemiluminescence (R = + 0.56, p = 0.0002). Luminol chemiluminescence was inhibited by sodium azide (-80%), catalase (-73%), and dimethyl sulphoxide (-24%). Superoxide dismutase inhibited lucigenin more than luminol dependent chemiluminescence (-61% and -7% respectively, p < 0.05). Within disease groups, Helicobacter pylori antral infection was associated with increased duodenal chemiluminescence, whereas smoking, alcohol, and use of NSAIDs or H2 blockers had no influence. Their disease related generation in duodenal mucosa supports a role for reactive oxygen metabolites in the pathogenesis of duodenitis and duodenal ulcer. These metabolites might include superoxide, hydrogen peroxide, hydroxyl, and products of myeloperoxidase activity.

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