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大鼠各种形式实验性急性肾小管坏死的早期事件。

Early events in various forms of experimental acute tubular necrosis in rats.

作者信息

Preuss H G, Tourkantonis A, Hsu C H, Shim P S, Barzyk P, Tio F, Schreiner G E

出版信息

Lab Invest. 1975 Mar;32(3):286-94.

PMID:1123911
Abstract

Metabolic and morphologic changes occurred in the kidneys of rats within 3 hours after inciting acute tubular necrosis by completely clamping the renal blood supply, by intramuscular injections of glycerol, and by subcutaneous injections of HgC12. Although the initial trend was for p-aminohippurate and tetraethylammonium transport to decrease and for oxygen consumption, ammonia production, and gluconeogenesis to increase after glycerol, all of these parameters changed in opposite directions after renal pedicle clamping and after subcutaneous HgC12 (4.7 mg. per kg;). In addition, early morphologic changes in glycerol-injected rats differed from those seen with pedicle clamping and low dose HgC12. With high dose HgC12 (25 mg. per kg.), the metabolic and morphologic changes were somewhere in between those seen with the other insults. Coinciding with early metabolic and morphologic changes, cardiac output and renal blood flow decreased soon after the glycerol was given. On the basis of our findings, we cannot ascribe all of the early metabolic and morphologic changes in the glycerol model to ischemia, and we postulate that the circulating heme proteins may be nephrotoxic to ischemic renal tissue.

摘要

通过完全夹闭肾血流、肌肉注射甘油以及皮下注射HgC12诱导大鼠急性肾小管坏死,3小时内大鼠肾脏发生了代谢和形态学变化。尽管在注射甘油后,对氨基马尿酸和四乙铵转运最初呈下降趋势,而氧消耗、氨生成和糖异生呈增加趋势,但在夹闭肾蒂和皮下注射HgC12(4.7毫克/千克)后,所有这些参数均呈相反方向变化。此外,注射甘油的大鼠早期形态学变化与夹闭肾蒂和低剂量HgC12所致变化不同。高剂量HgC12(25毫克/千克)时,代谢和形态学变化介于其他损伤所见变化之间。与早期代谢和形态学变化一致,注射甘油后不久心输出量和肾血流量下降。根据我们的研究结果,我们不能将甘油模型中的所有早期代谢和形态学变化都归因于缺血,我们推测循环中的血红素蛋白可能对缺血性肾组织具有肾毒性。

相似文献

1
Early events in various forms of experimental acute tubular necrosis in rats.大鼠各种形式实验性急性肾小管坏死的早期事件。
Lab Invest. 1975 Mar;32(3):286-94.
2
The morphology of "acute tubular necrosis" in man: analysis of 57 renal biopsies and a comparison with the glycerol model.人类“急性肾小管坏死”的形态学:57例肾活检分析及与甘油模型的比较
Medicine (Baltimore). 1979 Sep;58(5):362-76.
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Tubular function in experimental acute tubular necrosis in rats.大鼠实验性急性肾小管坏死中的肾小管功能
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Necrosis of the pars recta (S3 segment) of the rat kidney produced by hexachloro 1:3 butadiene.六氯-1:3-丁二烯导致的大鼠肾脏直部(S3段)坏死。
J Pathol. 1982 Oct;138(2):99-113. doi: 10.1002/path.1711380202.
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Toxicology and Carcinogenesis Studies of Ochratoxin A (CAS No. 303-47-9) in F344/N Rats (Gavage Studies).赭曲霉毒素A(CAS编号:303-47-9)在F344/N大鼠中的毒理学和致癌性研究(灌胃研究)
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Ischemic acute renal failure--pathogenetic steps leading to acute tubular necrosis.缺血性急性肾衰竭——导致急性肾小管坏死的发病机制步骤。
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Acute mercuric chloride nephrotoxicity. An electron microscopic and metabolic study.急性氯化汞肾毒性。一项电子显微镜及代谢研究。
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Phenylbutazone nephrotoxicity--a light and electron microscopic study.保泰松肾毒性——光镜和电镜研究
Ir J Med Sci. 1983 Dec;152(12):435-9. doi: 10.1007/BF02958705.
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Renal ammoniagenesis in kidney slices from rats undergoing glycerol-induced acute tubular necrosis.
Experientia. 1982 Jun 15;38(6):678. doi: 10.1007/BF01964090.
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Effect of the adenosine antagonist 8-phenyltheophylline on glycerol-induced acute renal failure in the rat.腺苷拮抗剂8-苯基茶碱对甘油诱导的大鼠急性肾衰竭的影响。
Br J Pharmacol. 1986 May;88(1):205-12. doi: 10.1111/j.1476-5381.1986.tb09488.x.
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Glomerular mesangial and endothelial cell swelling following temporary renal ischemia and its role in the no-reflow phenomenon.短暂性肾缺血后肾小球系膜细胞和内皮细胞肿胀及其在无复流现象中的作用。
Am J Pathol. 1977 Oct;89(1):153-66.
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Intra- and extrarenal vascular changes in the acute renal failure of the rat caused by mercury chloride.氯化汞所致大鼠急性肾衰竭时肾内和肾外血管的变化
Virchows Arch A Pathol Anat Histol. 1977 Jan 20;372(4):259-85. doi: 10.1007/BF00432403.