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一氧化氮在新生大鼠缺氧诱导变化中的作用。

Role of nitric oxide in hypoxia-induced changes in newborn rats.

作者信息

Kiliç I, Kiliç B A, Güven C, Demirpençe E, Akşit M A

机构信息

Department of Pediatrics, Pamukkale University Faculty of Medicine, Denizli, Turkey.

出版信息

Biol Neonate. 2000 Oct;78(3):191-7. doi: 10.1159/000014270.

DOI:10.1159/000014270
PMID:11044768
Abstract

In order to investigate the role of nitric oxide (NO) in hypoxic tissue damage in newborns, we studied the effects of systemic administration of an inhibitor of NO synthase, N(G)-nitro-L-arginine (L-NNA), and the precursor for the synthesis of NO, L-arginine (L-ARG), on the biochemical and histological changes in brain, heart, lung, liver, kidney, intestine, and skeletal muscle tissues. Four groups of 1-day-old Wistar rat pups were used: control, hypoxic, L-ARG, and L-NNA groups. L-ARG 100 mg/kg or L-NNA 2 mg/kg was administered as a bolus intraperitoneally 1.5 h before hypoxia. Hypoxia increased lipid peroxidation in all tissues except muscle; this increase was prevented by L-NNA and L-ARG in brain, heart, lung, kidney, and liver tissues. L-NNA in intestine and L-ARG in muscle tissue increased lipid peroxidation. The tissue-associated myeloperoxidase activity was decreased in the liver by L-NNA and L-ARG. Histopathological changes in intestines were villous epithelial separation and hyperemia in hypoxic and L-NNA groups which were not observed in control and L-ARG groups. In lungs, pulmonary hemorrhage was observed only in the hypoxic group. These data suggest that NO acts both as a destructive and a protective agent in the pathogenesis of hypoxia-reoxygenation injuries.

摘要

为了研究一氧化氮(NO)在新生儿缺氧性组织损伤中的作用,我们研究了全身给予一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸(L-NNA)以及一氧化氮合成前体L-精氨酸(L-ARG)对脑、心脏、肺、肝脏、肾脏、肠道和骨骼肌组织生化及组织学变化的影响。使用了四组1日龄的Wistar大鼠幼崽:对照组、缺氧组、L-ARG组和L-NNA组。在缺氧前1.5小时腹腔内推注给予100mg/kg的L-ARG或2mg/kg的L-NNA。缺氧增加了除肌肉外所有组织中的脂质过氧化;在脑、心脏、肺、肾脏和肝脏组织中,L-NNA和L-ARG可防止这种增加。肠道中的L-NNA和肌肉组织中的L-ARG增加了脂质过氧化。L-NNA和L-ARG降低了肝脏中与组织相关的髓过氧化物酶活性。肠道组织病理学变化在缺氧组和L-NNA组中表现为绒毛上皮分离和充血,而在对照组和L-ARG组中未观察到。在肺中,仅在缺氧组观察到肺出血。这些数据表明,在缺氧-复氧损伤的发病机制中,NO既起破坏作用又起保护作用。

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