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实验性内毒素血症中肾小球变化的序列:溶血性尿毒症综合征的一种可能模型。

Sequence of glomerular changes in experimental endotoxemia: a possible model of hemolytic uremic syndrome.

作者信息

Bertani T, Abbate M, Zoja C, Corna D, Remuzzi G

机构信息

Mario Negri Institute for Pharmacological Research, Bergamo, Italy.

出版信息

Nephron. 1989;53(4):330-7. doi: 10.1159/000185777.

DOI:10.1159/000185777
PMID:2601800
Abstract

Glomerular morphological changes produced by 5-hour intravenous infusion of endotoxin (40 micrograms/kg/h) were studied in 57 rabbits. During endotoxin infusion all animals developed signs of endotoxemia, anemia, and transient leukopenia and thrombocytopenia. Acute renal failure also developed in all animals. By light microscopy a marked polymorphonuclear cell infiltration was the prominent finding within 1 h from the beginning of the infusion. At hour 5 fibrin deposits and thrombi were detected in most animals. The abnormalities were reversible. By electron microscopy endothelial damage was detected few minutes after the beginning of endotoxin infusion followed by leukocyte and platelet infiltration in glomerular capillaries. Fibrin appeared at hour 5 as free strands into the lumens or in large clumps along the luminal surface of endothelial layer. Occasionally, occlusive fibrin thrombi were seen. At hour 48 only mild endothelial damage was seen, associated with few polymorphonuclear cells in the glomerular capillary lumens. These results document the sequence of renal changes in the best available animal model of hemolytic uremic syndrome. Beside endothelial damage, leukocyte infiltration in glomerular capillaries is a prominent finding suggesting a role of inflammatory cells in the development of microvascular thrombosis.

摘要

在57只兔子中研究了静脉内输注内毒素(40微克/千克/小时)5小时所产生的肾小球形态学变化。在内毒素输注期间,所有动物均出现内毒素血症、贫血以及短暂性白细胞减少和血小板减少的体征。所有动物也都出现了急性肾衰竭。通过光学显微镜观察,在输注开始后1小时内,明显的多形核细胞浸润是突出的发现。在第5小时,大多数动物检测到纤维蛋白沉积和血栓形成。这些异常是可逆的。通过电子显微镜观察,在内毒素输注开始几分钟后检测到内皮损伤,随后肾小球毛细血管出现白细胞和血小板浸润。在第5小时,纤维蛋白以游离束状形式出现在管腔内或沿内皮细胞层腔面形成大团块。偶尔可见闭塞性纤维蛋白血栓。在第48小时,仅见轻度内皮损伤,伴有肾小球毛细血管腔内少量多形核细胞。这些结果记录了溶血性尿毒症综合征现有最佳动物模型中肾脏变化的顺序。除内皮损伤外,肾小球毛细血管内白细胞浸润是一个突出的发现,提示炎症细胞在微血管血栓形成中起作用。

相似文献

1
Sequence of glomerular changes in experimental endotoxemia: a possible model of hemolytic uremic syndrome.实验性内毒素血症中肾小球变化的序列:溶血性尿毒症综合征的一种可能模型。
Nephron. 1989;53(4):330-7. doi: 10.1159/000185777.
2
Tumor necrosis factor induces glomerular damage in the rabbit.肿瘤坏死因子可诱导家兔肾小球损伤。
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Alternative pathway activation of complement by Shiga toxin promotes exuberant C3a formation that triggers microvascular thrombosis.志贺毒素通过替代途径激活补体促进丰富的 C3a 形成,从而引发微血管血栓形成。
J Immunol. 2011 Jul 1;187(1):172-80. doi: 10.4049/jimmunol.1100491. Epub 2011 Jun 3.
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Neutrophil function in an experimental model of hemolytic uremic syndrome.溶血尿毒症综合征实验模型中的中性粒细胞功能
Pediatr Res. 1987 Mar;21(3):252-6. doi: 10.1203/00006450-198703000-00009.
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Impaired and exhausted platelets in modified generalized Shwartzman reaction: an analogue of hemolytic uremic syndrome associated with endotoxemia.改良型全身性施瓦茨曼反应中受损和耗竭的血小板:一种与内毒素血症相关的溶血性尿毒症综合征的类似物。
J Lab Clin Med. 1983 Dec;102(6):847-57.
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Mitomycin-induced hemolytic-uremic syndrome.丝裂霉素诱导的溶血尿毒综合征。
Arch Pathol Lab Med. 1984 Dec;108(12):959-62.
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Hemolytic uremic syndrome with hypocomplementemia, serum C3NeF, and glomerular deposits of C3.伴有低补体血症、血清C3NeF及C3肾小球沉积物的溶血性尿毒症综合征
Arch Pathol Lab Med. 1977 Jul;101(7):357-61.
8
Mitomycin-induced hemolytic uremic kidney. An experimental model in the rat.丝裂霉素诱导的溶血性尿毒症性肾病。大鼠实验模型。
Am J Pathol. 1985 Oct;121(1):88-95.
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Electron microscopic observations of the kidney in the generalized Shwartzman reaction.全身性施瓦茨曼反应时肾脏的电子显微镜观察。
Virchows Arch A Pathol Anat Histol. 1977 Jun 23;374(3):183-96. doi: 10.1007/BF00427113.
10
[Kidney morphology in hemolytic-uremic syndrome].
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