Role of prostaglandin deficiency in pathogenetic mechanism of gastric lesions induced by indomethacin in rats
Role of prostaglandin deficiency in pathogenetic mechanism of gastric lesions induced by indomethacin in rats
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前列腺素缺乏在吲哚美辛致大鼠胃损伤发病机制中的作用
DOI：
10.1007/bf01540340
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发表时间：
1989
影响因子：
3.1
通讯作者：
S. Okabe
中科院分区：
文献类型：
--
作者：
M. Okada;H. Niida;K. Takeuchi;S. Okabe
本研究在大鼠中进行，使用2-脱氧-D-葡萄糖（2DG）作为胃动力刺激剂和低剂量吲哚美辛作为前列腺素（PG）合成抑制剂，以研究胃动力和PG缺乏在吲哚美辛引起的胃损伤发病机制中的作用。皮下注射 5 mg/kg 吲哚美辛在 4 小时内不会引起粘膜任何明显损伤，但 25 mg/kg 剂量会产生沿胃长轴的线性出血损伤。静脉内给予2DG（100毫克/千克/小时），沿粘膜皱襞产生线性非出血性损伤，并且在存在5毫克/千克吲哚美辛的情况下，在胃的相同区域引起严重出血性损伤。吲哚美辛 (25 mg/kg) 和 2DG 均显着增强胃动力，而仅后者增加胃酸排出量和粘膜血流量。吲哚美辛 (25 mg/kg) 显着降低粘膜 PGE2 水平，但 2DG 则没有显着降低粘膜 PGE2 水平。单独使用 5 mg/kg 吲哚美辛对除 PG 水平以外的任何参数均没有影响或影响很小，PG 水平降低的程度与 25 mg/kg 该药物引起的程度相似。病变的时程发展与给予吲哚美辛（25 mg/kg）和2DG后胃动力的变化密切相关。这些结果表明，胃动力增强本身足以引起粘膜损伤（非出血性），而单独的 PG 缺乏不会引起任何损伤，但需要进一步扩展到最初由胃动力增强引起的非出血性病变的出血性病变。
The present study was undertaken in rats using 2-deoxy-D-glucose (2DG) as a stimulator of gastric motility and a low dose of indomethacin as a prostaglandin (PG) synthesis inhibitor to investigate the roles of gastric motility and PG deficiency in the pathogenesis of indomethacin-induced gastric lesions. Subcutaneously administered indomethacin at 5 mg/kg did not induce any visible damage in the mucosa within 4 hr, but at 25 mg/kg produced linear hemorrhagic lesions along the long axis of the stomach. 2DG (100 mg/kg/hr), given intravenously, produced linear nonhemorrhagic lesions along the mucosal folds and, in the presence of 5 mg/kg of indomethacin, caused severe hemorrhagic lesions in the same areas of the stomach. Gastric motility was markedly enhanced by both indomethacin (25 mg/kg) and 2DG, while acid output and mucosal blood flow were increased only by the latter. Mucosal PGE2levels were significantly reduced by indomethacin (25 mg/kg) but not by 2DG. Indomethacin at 5 mg/kg alone had no or little effect on any parameter except PG levels, which were reduced to similar degrees as caused by 25 mg/kg of the agent. Time-course development of the lesions was closely associated with those changes in gastric motility after administration of indomethacin (25 mg/kg) and 2DG. These results suggest that the enhanced gastric motility is, by itself, sufficient to induce damage (nonhemorrhagic) in the mucosa and that a PG deficiency alone does not induce any damage but is required for further extension to hemorrhagic lesions of nonhemorrhagic ones that are initially induced by enhanced gastric motility.
融合多元智能理论、以真实体验理解为目标的科学学习
DOI：
--
发表时间：
2010
期刊：
日本教科教育学会第36回全国大会論文集
影响因子：
--
作者：
Ryoko KODAMA;Miho KATO;Mariko ISHIGURO;玉村かおり・松本伸示
通讯作者：
玉村かおり・松本伸示