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腺苷在肠缺血再灌注损伤期间对硝基蓝四氮唑沉积及表面pH的作用

Actions of adenosine on nitro blue tetrazolium deposition and surface pH during intestinal reperfusion injury.

作者信息

Kaminski P M, Proctor K G

机构信息

Department of Physiology and Biophysics, University of Tennessee Health Science Center, Memphis 38163.

出版信息

Circ Res. 1990 Jun;66(6):1713-9. doi: 10.1161/01.res.66.6.1713.

Abstract

Mesenteric arteries supplying an intestinal segment were occluded for 5 minutes and then released. During reperfusion, two series of measurements were made with various substances topically applied to the extraluminal surface. In the first series, reduced nitro blue tetrazolium (NBT) was extracted from tissue and measured spectrophotometrically, as an index of oxidative damage. In the second series, mucosal and serosal surface pH was measured as an index of the functional ability to maintain ion gradients. In control conditions, NBT deposition averaged 55-63 micrograms/g tissue. After 60 and 120 minutes of reperfusion, NBT was elevated to 446-479 micrograms/g, which was approximately half as large as the NBT increment (846 micrograms/g) produced by a 15-minute application of xanthine plus xanthine oxidase to well-perfused tissue. As expected, NBT levels were significantly lower (299 micrograms/g) in tissue that was continuously suffused with superoxide dismutase (SOD) plus catalase (CAT) before occlusion and during reperfusion. Similar NBT levels (274 micrograms/g) were observed after reperfusion in animals that were fed a diet supplemented with the antioxidant vitamin E for 4-6 weeks. These observations affirm that some, but not all, NBT deposition after reperfusion can be attributed to oxyradicals. However, with exogenous adenosine (ADO) applied for the first 30 minutes after occlusion, NBT was elevated to 174 micrograms/g after 60 minutes, which was only half as large as the increment with SOD plus CAT, even though those substances were continuously applied. The opposite effect was produced by an ADO receptor antagonist, 8-phenyltheophylline; NBT was increased to 516 micrograms/g.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

供应一段肠段的肠系膜动脉被阻断5分钟后再松开。在再灌注期间,对局部应用于肠腔外表面的各种物质进行了两组测量。在第一组中,从组织中提取还原型硝基蓝四氮唑(NBT)并通过分光光度法进行测量,作为氧化损伤的指标。在第二组中,测量黏膜和浆膜表面的pH值,作为维持离子梯度功能能力的指标。在对照条件下,NBT沉积平均为55 - 63微克/克组织。再灌注60分钟和120分钟后,NBT升高至446 - 479微克/克,这大约是在灌注良好的组织中应用黄嘌呤加黄嘌呤氧化酶15分钟所产生的NBT增量(846微克/克)的一半。正如预期的那样,在阻断前和再灌注期间持续灌注超氧化物歧化酶(SOD)加过氧化氢酶(CAT)的组织中,NBT水平显著较低(299微克/克)。在喂食补充抗氧化剂维生素E 4 - 6周的动物再灌注后观察到类似的NBT水平(274微克/克)。这些观察结果证实,再灌注后部分但并非全部的NBT沉积可归因于氧自由基。然而,在阻断后最初30分钟应用外源性腺苷(ADO),60分钟后NBT升高至174微克/克,尽管持续应用了SOD加CAT,但其增量仅为它们的一半。腺苷受体拮抗剂8 - 苯基茶碱产生了相反的效果;NBT增加到516微克/克。(摘要截断于250字)

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