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急性肾衰竭兔脾损伤的机制。

The mechanism of spleen injury in rabbits with acute renal failure.

机构信息

Institute of Microcirculation, Hebei North University, Zhangjiakou 075000, Hebei, PR China.

出版信息

Ren Fail. 2011;33(4):418-25. doi: 10.3109/0886022X.2011.568145.

DOI:10.3109/0886022X.2011.568145
PMID:21529271
Abstract

Immune function disorders are common during acute renal failure (ARF), but the mechanisms are unknown. As the spleen is the largest organ of the immune system, we aimed to observe if there are morphological changes in the spleen in rabbits with ARF. In addition, we tried to explore its mechanism from the perspective of oxygen free radicals, nitric oxide (NO), myeloperoxidase (MPO), and membrane pump activities. ARF animal models were established by either hypodermic injection of 1.3 mL/kg bw 1% HgCl₂ or intramuscular injection of 10 mL/kg bw 50% glycerin. Animals were divided into 12 h, 24 h, and 48 h treatment groups with six rabbits in each group. Compared with control animals, congestion was found in the spleen and splenic trabeculae were increased in the two ARF model groups at multiple time points. The malonaldehyde, NO, nitric oxide synthase, and MPO levels in the ARF models were increased compared with the control group at 24 h or 48 h, and the superoxide dismutase and adenosine triphosphatase activities were significantly lower than the levels in the control group at multiple time points. These indices of free radical damage were induced gradually with ARF development, and there were statistically significant differences at different time points. These data suggested that histological damage of spleen during ARF may lead to immune disorders, which might be related to free radical injury, NO excessive release, polymorphonuclear neutrophils (PMN) sequestration, and membrane pump dysfunction.

摘要

免疫功能障碍在急性肾衰竭(ARF)期间很常见,但机制尚不清楚。由于脾脏是最大的免疫系统器官,我们旨在观察 ARF 兔脾脏是否存在形态学变化。此外,我们试图从氧自由基、一氧化氮(NO)、髓过氧化物酶(MPO)和膜泵活性的角度探讨其机制。通过皮下注射 1.3 mL/kg bw 1% HgCl₂或肌肉注射 10 mL/kg bw 50%甘油分别建立 ARF 动物模型。动物分为 12 h、24 h 和 48 h 治疗组,每组 6 只兔子。与对照组相比,在两个 ARF 模型组的多个时间点发现脾脏充血,脾小梁增加。与对照组相比,在 24 小时或 48 小时,ARF 模型中的丙二醛、NO、一氧化氮合酶和 MPO 水平升高,超氧化物歧化酶和三磷酸腺苷酶活性在多个时间点显著低于对照组。这些自由基损伤指标随着 ARF 的发展逐渐被诱导,并且在不同时间点存在统计学差异。这些数据表明,ARF 期间脾脏的组织学损伤可能导致免疫功能障碍,这可能与自由基损伤、NO 过度释放、多形核白细胞(PMN)聚集和膜泵功能障碍有关。

相似文献

1
The mechanism of spleen injury in rabbits with acute renal failure.急性肾衰竭兔脾损伤的机制。
Ren Fail. 2011;33(4):418-25. doi: 10.3109/0886022X.2011.568145.
2
The mechanism of myocardium and pancreas injury in rabbits with acute renal failure might be related to myeloperoxidase and membrane pump activities.兔急性肾功能衰竭时心肌和胰腺损伤的机制可能与髓过氧化物酶和膜泵活性有关。
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The protective effect of nebivolol on ischemia/reperfusion injury in rabbit spinal cord.奈必洛尔对兔脊髓缺血/再灌注损伤的保护作用。
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[The protective efficacy of rabbit endogenous nitric oxide against acute rabbit lung ischemia-reperfusion injury and its mechanism].[兔内源性一氧化氮对兔急性肺缺血再灌注损伤的保护作用及其机制]
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引用本文的文献

1
Mesenteric lymph reperfusion exacerbates spleen injury caused by superior mesenteric artery occlusion shock.肠系膜淋巴再灌注会加剧由肠系膜上动脉闭塞性休克引起的脾脏损伤。
Braz J Med Biol Res. 2014 May;47(5):376-83. doi: 10.1590/1414-431x20143639. Epub 2014 May 2.
2
Mesenteric lymph drainage alleviates acute kidney injury induced by hemorrhagic shock without resuscitation.肠系膜淋巴引流可缓解失血性休克未复苏所致的急性肾损伤。
ScientificWorldJournal. 2014 Feb 25;2014:720836. doi: 10.1155/2014/720836. eCollection 2014.