Hillman B J, Hollenberg N K, Mellins H Z
Invest Radiol. 1979 Sep-Oct;14(5):415-20. doi: 10.1097/00004424-197909000-00006.
Studies showing diminished cortical perfusion and reduced glomerular filtration in acute renal failure are apparently at odds with reports of a persistent nephrogram during urography in this disease. We followed the progression of nephrograms in eight dehydrated normal rats, in seven dehydrated rats treated with 12 mg/kg of mercuric chloride (nephrotoxic acute renal failure), and in nine dehydrated rats receiving 5 g/kg of IM-glycerol (myoglobinuric acute renal failure). To assess the capacity of our technique to identify a persistent, dense nephrogram, hemorrhagic hypotension (mean arterial pressure, 55-70 mm Hg) was induced in three rats. All rats showed nephrograms on magnification radiographs 1 minute following the injection of 1 cc/lb of sodium diatrizoate. Duplicate coded readings showed no prolongation of nephrograms in ARF-affected animals. Only the hypotensive rats manifested nephrograms on 2-hour radiographs. Some differing characteristics of nephrograms among the groups are explainable on the basis of differences in renal blood flow, as determined in separate experiments. Our findings would favor a preglomerular mechanism as the cause of oliguria in acute renal failure.
研究表明,急性肾衰竭时皮质灌注减少和肾小球滤过率降低,这显然与该病尿路造影时持续肾影的报道相矛盾。我们跟踪观察了8只脱水正常大鼠、7只经12mg/kg氯化汞处理的脱水大鼠(肾毒性急性肾衰竭)以及9只接受5g/kg肌内注射甘油的脱水大鼠(肌红蛋白尿性急性肾衰竭)肾影的变化过程。为评估我们的技术识别持续浓密肾影的能力,对3只大鼠诱发了出血性低血压(平均动脉压55 - 70mmHg)。所有大鼠在注射1cc/lb泛影酸钠1分钟后的放大X光片上均显示有肾影。重复的编码读数显示,受急性肾衰竭影响的动物肾影无延长。只有低血压大鼠在2小时X光片上显示有肾影。根据在单独实验中测定的肾血流量差异,各实验组肾影的一些不同特征是可以解释的。我们的研究结果支持将肾前机制作为急性肾衰竭少尿的原因。