实验性尿毒症大鼠肝脏灌注合成尿素。

G Perez, B Rietberg, B Owens, T Parker, H Obaya, E Schiff
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引用次数: 5

摘要

为了严格控制给肝的底物(NH4Cl),采用离体灌注大鼠肝脏对实验性尿毒症尿素合成进行了检测。研究前48小时,雌性Sprague-Dawley大鼠双侧肾切除术(n = 7)造成急性尿毒症。7只大鼠右肾切除术和左肾节段性梗死引起慢性尿毒症(8 ~ 14周)。在NH4Cl输注速率(8.3 μ mol/min)导致肝前灌注氨水平约为先前描述的Km值的两倍时,慢性尿毒症大鼠的肝脏尿素生成率略高于对照组(对照组:0.41 +/- 0.03;慢性尿毒症:湿肝重0.54±0.04 μ mol/min/g;P < 0.02)。急性尿毒症大鼠尿素产量(0.66 +/- 0.05 mumol/min/g)高于假手术大鼠(0.59 +/- 0.05 mumol/min/g),但差异无统计学意义。同时进行的牛磺胆酸盐转运研究没有发现尿毒症动物和对照动物肝脏之间的显著功能差异。数据表明,与对照动物相比,尿毒症大鼠肝脏的尿素产量增加。
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Urea synthesis by perfused rat liver in experimental uremia.

Urea synthesis was examined in experimental uremia using the isolated perfused rat liver in order to assure strict control of substrate (NH4Cl) presented to the liver. Acute uremia was created in female Sprague-Dawley rats by bilateral nephrectomy (n = 7) 48 h prior to studies. Chronic uremia (8--14 weeks) was produced by right nephrectomy and segmental infarction of the left kidney in 7 rats. At infusion rates of NH4Cl (8.3 mumol/min) which resulted in prehepatic perfusate ammonia levels approximately twice the previously described Km value, livers of chronically uremic rats had slightly higher rates of urea production than controls (controls: 0.41 +/- 0.03; chronic uremia: 0.54 +/- 0.04 mumol/min/g of wet liver weight; p less than 0.02). In acute uremia, urea production was higher (0.66 +/- 0.05 mumol/min/g) than in sham-operated rats (0.59 +/- 0.05 mumol/min/g) but the differences did not achieve statistical significance. Simultaneously performed taurocholate transport studies did not reveal significant functional differences between the livers of uremic and control animals. The data suggest that urea production by livers of uremic rats is increased when compared to that of control animals.

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