RENAL EFFECTS OF RADIOCONTRAST AGENTS IN RATS - A NEW MODEL OF ACUTE-RENAL-FAILURE
RENAL EFFECTS OF RADIOCONTRAST AGENTS IN RATS - A NEW MODEL OF ACUTE-RENAL-FAILURE
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DOI：
10.1159/000168177
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发表时间：
1990-11-01
影响因子：
4.2
通讯作者：
JACOBS, C
中科院分区：
文献类型：
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作者：
DERAY, G;DUBOIS, M;JACOBS, C
本研究的目的是首先建立一种可重复性和可逆性的大鼠注射造影剂后急性肾功能衰竭的模型；其次，使用该方法比较低渗透和高渗透压造影剂的肾毒性。在主动脉内注入造影剂或生理盐水，同时在肾动脉上方的主动脉上应用夹子。肾缺血3min加或不加等渗盐水后，血肌酐无明显变化，24 h内生肌酐清除率略有下降，尿N-乙酰氨基葡萄糖苷酶(NAG)排泄量未见改变。检查的17个肾脏均为正常。2,100 mom/kg高渗盐水组血清肌酐显著升高，内生肌酐清除率显著降低(24和48 h分别由1.8±0.1降至0.8+/-0.1和1.0+/-0.2ml/min)。24 h和48 h尿NAG排泄量分别从23+/-18增加到48+/-20和8+/-4-mU-molh-1/mmolScinine(p<；0.05)。5例肾组织学检查显示急性肾小管坏死3例，无组织学异常2例。泛影葡胺引起急性可逆性肾功能衰竭。肌酐清除率分别从1.6+/-0.1降至0.4+/-和0.8+/-0.1ml/min(p<；0.01)。24 h和48 h尿NAG排泄量分别由43+/-9增加到352+/-79和+/-23 mU·molh-1/mmolScinine。7例肾组织学检查发现急性肾小管坏死4例，肾小管细胞胞浆空泡化2例，无组织学异常1例。与对照组相比，异沙格酸盐和异丙咪醇对血肌酐没有影响，而对内生肌酐清除率有轻微的影响。Ioxagate和Iopamidol在24 h引起尿NAG排泄量显著增加(Ioxagate：31+/-6至147+/-31；Iopamidol：55+/-20至123+/-31 mU·molh-1/mmolcreatinine)，48h完全可逆(Ioxagate：31+/-9；Iopamidol：41+/-8)。8个肾的组织学分析显示肾小管上皮细胞胞浆空泡化(n=7)，无组织学异常(n=1)。10例肾组织学检查显示肾小管上皮细胞胞浆空泡化(n=8)，未见组织学异常(n=2)。我们描述了一种可重复性和可逆性的造影剂诱导的大鼠急性肾功能衰竭模型。在该模型中，离子型和非离子型低渗造影剂的肾毒性低于高渗型造影剂。
The objectives of this study were first to develop a reproducible and reversible model of acute renal failure following contrast medium infusion in the rat; second to use that method to compare the nephrotoxicity of low- and high-osmolar contrast agents. Contrast media or saline were perfused in the aorta while a clamp was applied on the aorta just above the renal artery. Three minutes of renal ischemia with or without infusion of isotonic saline induced no change in serum creatinine and a slight and transient decrease in creatinine clearance at 24 h. Urinary N-acetyl glucosamidase (NAG) excretion was not modified in this control group. All 17 kidneys which were examined were normal. 2,100 mosm/kg hypertonic saline induced a significant increase in serum creatinine and a significant decrease in creatinine clearance (from 1.8 +/- 0.1 to 0.8 +/- 0.1 and 1.0 +/- 0.2 ml/min at 24 and 48 h, respectively). Urinary NAG excretion increased from 23 +/- 18 to 48 +/- 20 and 8 +/- 4-mu-mol h-1/mmol creatinine at 24 and 48 h, respectively (p < 0.05). Histologic analysis of 5 kidneys revealed acute tubular necrosis (n = 3) and no histologic abnormalities (n = 2). Diatrizoate induced an acute and reversible renal failure. Creatinine clearance decreased from 1.6 +/- 0.1 to 0.4 +/- and 0.8 +/- 0.1 ml/min at 24 and 48 h, respectively (p < 0.01). Urinary NAG excretion increased also significantly from 43 +/- 9 to 352 +/- 79 and 64 +/- 23-mu-mol h-1/mmol creatinine at 24 and 48 h, respectively. Histologic examination of 7 kidneys revealed acute tubular necrosis (n = 4), tubular cytoplasmic vacuolization (n = 2), and no histologic abnormalities (n = 1). Ioxaglate and iopamidol induced no change in serum creatinine and a slight decrease in creatinine clearance comparable to that observed in the control group. Ioxaglate and iopamidol induced a significant increase in urinary NAG excretion at 24 h (ioxaglate: 31 +/- 6 to 147 +/- 31; iopamidol: 55 +/- 20 to 123 +/- 31-mu-mol h-1/mmol creatinine) which was completely reversible at 48 h (ioxaglate: 31 +/- 9; iopamidol: 41 +/- 8). Histological analysis of 8 kidneys exposed to ioxaglate revealed tubular cytoplasmic vacuolisation (n = 7) and no histologic abnormalities (n = 1). Histological analysis of 10 kidneys exposed to iopamidol revealed tubular cytoplasmic vacuolization (n = 8) and no histologic abnormalities (n = 2). We have described a reproducible and reversible model of contrast-medium-induced acute renal failure in the rat. In this model, ionic and nonionic low-osmolar contrast agents are less nephrotoxic than high-osmolar contrast agents.