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超氧化物:缺血性肠损伤中的一种关键氧自由基。

Superoxide: a critical oxygen-free radical in ischemic bowel injury.

作者信息

Dunn S P, Gross K R, Dalsing M, Hon R, Grosfeld J L

出版信息

J Pediatr Surg. 1984 Dec;19(6):740-4. doi: 10.1016/s0022-3468(84)80361-9.

DOI:10.1016/s0022-3468(84)80361-9
PMID:6097660
Abstract

The radical anions of molecular oxygen reduction, superoxide (O2), hydrogen peroxide (H2O2), and hydroxyl radical (OH), have been implicated in a number of disease processes, including ischemic bowel injury. This report evaluates the effect of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO), selenium treatment, and selenium deficiency on bowel integrity and survival in experimental intestinal ischemia in rats. Ischemic bowel injury was produced in 204 male Sprague-Dawley rats (wt 90 to 100 g) by a one-minute occlusion of the superior mesenteric artery (SMA) with a microaneurysm clip. Experiment I treatment animals (n = 20) received 2.5 mg/kg SOD dissolved in Ringer's lactate, and control animals (n = 71) received Ringer's lactate alone. Experiment II treatment animals (n = 16) received 1 cc of 100% DMSO gavage, and control animals (n = 11) received no treatment. Experiment III treatment animals (n = 17) received 25 mg/kg CAT dissolved in phosphate buffered saline, and control animals (n = 11) received nothing. Experiment IV treatment animals (n = 14) received 300 micrograms of sodium selenate by gavage dissolved in deionized water, and control animals (n = 15) receiving nothing. Experiment V treatment animals (n = 20) were raised from 35 to 50 g size on a selenium deficient diet, and control animals were raised (n = 20) on a normal rat chow diet, until they weighed 100 g when ischemia was induced. At seven days, survival, incidence of bowel perforation or necrosis, and length of survival were compared in each experiment between control and treatment groups using chi 2 analysis.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

分子氧还原产生的自由基阴离子,如超氧阴离子(O₂)、过氧化氢(H₂O₂)和羟基自由基(OH),与包括缺血性肠损伤在内的多种疾病过程有关。本报告评估了超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、二甲基亚砜(DMSO)、硒处理以及硒缺乏对大鼠实验性肠缺血时肠完整性和存活率的影响。通过用微动脉瘤夹夹闭肠系膜上动脉(SMA)1分钟,在204只雄性Sprague-Dawley大鼠(体重90至100克)中造成缺血性肠损伤。实验I中,治疗组动物(n = 20)接受溶解于乳酸林格氏液中的2.5毫克/千克SOD,对照组动物(n = 71)仅接受乳酸林格氏液。实验II中,治疗组动物(n = 16)接受1毫升100% DMSO灌胃,对照组动物(n = 11)未接受治疗。实验III中,治疗组动物(n = 17)接受溶解于磷酸盐缓冲盐水中的25毫克/千克CAT,对照组动物(n = 11)未接受任何处理。实验IV中,治疗组动物(n = 14)接受溶解于去离子水中的300微克硒酸钠灌胃,对照组动物(n = 15)未接受任何处理。实验V中,治疗组动物(n = 20)在缺硒饮食下从35克饲养至50克,对照组动物(n = 20)以正常大鼠饲料饲养,直至体重达到100克时诱导缺血。在第7天,使用卡方分析比较每个实验中对照组和治疗组之间的存活率、肠穿孔或坏死发生率以及存活时长。(摘要截断于250字)

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BMC Pediatr. 2014 Sep 10;14:226. doi: 10.1186/1471-2431-14-226.
2
Models of the pathogenesis of necrotizing enterocolitis.坏死性小肠结肠炎的发病机制模型
J Pediatr. 1990 Jul;117(1 Pt 2):S2-5. doi: 10.1016/s0022-3476(05)81123-0.