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慢性肝病患者利尿过程中腹水蛋白浓度升高的机制。

The mechanism of ascitic fluid protein concentration increase during diuresis in patients with chronic liver disease.

作者信息

Hoefs J C

出版信息

Am J Gastroenterol. 1981 Nov;76(5):423-31.

PMID:7337129
Abstract

The mechanism of increase in the protein concentration of ascitic fluid during diuresis was investigated in 27 patients with chronic liver disease. The albumin concentration increased in ascites from .58 +/- .49 gm.% in the initial paracentesis to 1.48 +/- .69 gm.% in the final paracentesis (P less than .001) as the serum albumin concentration increased from 2.40 +/- .44 gm.% 2.94 +/- .56 gm.% (P less than .001). The serum to ascites albumin concentration gradient decreased significantly from 1.82 +/- .39 gm.%-1.46 +/- .45 gm.% (P less than .001). Despite this decrease, the serum to ascites albumin concentration gradient was relatively constant (decrease of .36 gm.% or 20% of initial value) compared to either the absolute or percentage change in ascites total protein concentration (increase of 1.48 gm.% or 107% of initial value). In four patients studied prospectively, the plasma volume did not change (3.53 +/- .80 1.-3.73 +/- .59 1.) during diuresis, despite increase in total intravascular albumin (85.7 +/- 25.6 gm.-99.9 +/- 22.3 gm.; P less than .05) and decrease in total albumin in combined intravascular and peritoneal compartments (156.0 +/- 30.1 gm.-143.4 +/- 35.3 gm.; P less than .05). Since neither concentration without decrease in plasma volume or synthesis of protein without increase in total compartmental protein appear to be the major mechanism of serum protein concentration increase, the increase in serum protein concentration was attributed to redistribution of protein from ascites to the intravascular compartment. The increase in ascitic fluid protein concentration during diuresis can be attributed to an increase in serum protein concentration in the presence of the relatively stable serum to ascites albumin concentration gradient.

摘要

对27例慢性肝病患者利尿过程中腹水蛋白浓度升高的机制进行了研究。随着血清白蛋白浓度从2.40±0.44克%升高至2.94±0.56克%(P<0.001),腹水白蛋白浓度从首次腹腔穿刺时的0.58±0.49克%升高至末次腹腔穿刺时的1.48±0.69克%(P<0.001)。血清与腹水白蛋白浓度梯度从1.82±0.39克%-1.46±0.45克%显著降低(P<0.001)。尽管有这种降低,但与腹水总蛋白浓度的绝对值或百分比变化(升高1.48克%或初始值的107%)相比,血清与腹水白蛋白浓度梯度相对恒定(降低0.36克%或初始值的20%)。在4例前瞻性研究的患者中,利尿过程中血浆量未发生变化(3.53±0.80升-3.73±0.59升),尽管血管内总白蛋白增加(85.7±25.6克-99.9±22.3克;P<0.05),且血管内和腹腔内联合区域的总白蛋白减少(156.0±30.1克-143.4±35.3克;P<0.05)。由于血浆量不减少时浓度的变化以及总区域蛋白不增加时蛋白质合成的变化似乎都不是血清蛋白浓度升高的主要机制,因此血清蛋白浓度的升高归因于蛋白质从腹水向血管内区域的重新分布。利尿过程中腹水蛋白浓度的升高可归因于在血清与腹水白蛋白浓度梯度相对稳定的情况下血清蛋白浓度的升高。

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