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肠道缺血对大鼠肠道组织和血液中二胺氧化酶活性的影响。

Effect of intestinal ischemia on diamine oxidase activity in rat intestinal tissue and blood.

作者信息

Wollin A, Navert H, Bounous G

出版信息

Gastroenterology. 1981 Feb;80(2):349-55.

PMID:6778762
Abstract

This study examines the effect of increasing duration of intestinal ischemia on the mucosal integrity and the release of the enzyme diamine oxidase from the small intestine. Acute ischemia was produced by the occlusion of the superior mesenteric artery, and the subsequent changes in DNA and 125I-albumin content in the lumen were taken as indices of intestinal lesions. Diamine oxidase activity was measured in the intestinal lumen, mucosa, lymph, and serum. Occlusions of the superior mesenteric artery for periods of more than 60 min resulted in significant leakage of 125I-albumin (i.v.) into the lumen. In contrast, luminal DNA content rose significantly after 15 min of ischemia and continued to increase proportionally with the increased duration of the occlusion up to 120 min. Similarly, diamine oxidase activity was augmented in the lumen after 15 min of occlusion and rose sharply as the ischemic period was lengthened up to 60 min, leveling off thereafter. Increases in the diamine oxidase activity were also observed in the intestinal lymph and serum, reaching levels that were 2.6 and 3.6 times that of the control respectively after 60 min of ischemia. These findings suggest that intestinal ischemia reduces the diamine oxidase content in the intestinal mucosa by desquamation of the surface epithelial cells and by releasing the enzyme into the intestinal interstitial fluid, from which at least a portion is transported to the blood via the lymphatics. The early release of diamine oxidase seems to occur before the mucosal barrier is broken.

摘要

本研究探讨肠缺血持续时间延长对小肠黏膜完整性及二胺氧化酶释放的影响。通过阻断肠系膜上动脉制造急性缺血,将肠腔内DNA和125I-白蛋白含量的后续变化作为肠损伤指标。测定肠腔、黏膜、淋巴和血清中的二胺氧化酶活性。肠系膜上动脉阻断超过60分钟会导致125I-白蛋白(静脉注射)显著漏入肠腔。相反,缺血15分钟后肠腔DNA含量显著升高,并随着阻断时间延长至120分钟而持续成比例增加。同样,阻断15分钟后肠腔内二胺氧化酶活性增强,随着缺血时间延长至60分钟急剧上升,此后趋于平稳。在肠淋巴和血清中也观察到二胺氧化酶活性增加,缺血60分钟后分别达到对照水平的2.6倍和3.6倍。这些发现表明,肠缺血通过表面上皮细胞脱落以及将该酶释放到肠间质液中,从而降低肠黏膜中二胺氧化酶含量,其中至少一部分通过淋巴管转运到血液中。二胺氧化酶的早期释放似乎发生在黏膜屏障被破坏之前。

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