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肝硬化腹水形成的病理生理学

Pathophysiology of ascites formation in cirrhosis of the liver.

作者信息

Gerbes A L

机构信息

Department of Medicine II, Klinikum Grosshadern, University of Munich, F.R.G.

出版信息

Hepatogastroenterology. 1991 Oct;38(5):360-4.

PMID:1765351
Abstract

Current concepts of the pathophysiology of ascites formation in cirrhosis of the liver have become more complex. Traditionally, the initiating event of renal sodium and water retention in cirrhosis was considered to be ascites formation ("underfilling" hypothesis) or primary renal dysfunction ("overflow" hypothesis). Changes in systemic, splanchnic and renal hemodynamics, as well as of volume regulating hormones observed in cirrhosis are compatible with a decrease in effective blood volume as suggested by the "underfilling" hypothesis. These changes, however, have been shown to precede ascites formation. This observation, together with the demonstration of an increase in total blood volume in cirrhosis prompted the "overflow" hypothesis. However, many studies are incompatible with this concept and, in addition, the agent causing primary renal sodium retention in cirrhosis still remains to be defined. The recently proposed "vasodilation" hypothesis reconciles the most salient features of both theories, proposing peripheral arterial vasodilation as the initiating event of decreased effective blood volume and renal sodium retention. Further studies are needed to elucidate the temporal relationship and more precisely define the character of hemodynamic, humoral and renal changes in cirrhosis of the liver.

摘要

目前关于肝硬化腹水形成的病理生理学概念变得更加复杂。传统上,肝硬化时肾钠和水潴留的起始事件被认为是腹水形成(“充盈不足”假说)或原发性肾功能障碍(“溢流”假说)。肝硬化时观察到的全身、内脏和肾脏血流动力学以及容量调节激素的变化与“充盈不足”假说所提出的有效血容量减少相一致。然而,这些变化已被证明先于腹水形成。这一观察结果,连同肝硬化时总血容量增加的证明,促使了“溢流”假说的提出。然而,许多研究与这一概念不符,此外,导致肝硬化时原发性肾钠潴留的因素仍有待确定。最近提出的“血管舒张”假说调和了两种理论的最显著特征,提出外周动脉血管舒张是有效血容量减少和肾钠潴留的起始事件。需要进一步研究以阐明时间关系,并更精确地确定肝硬化时血流动力学、体液和肾脏变化的特征。

相似文献

1
Pathophysiology of ascites formation in cirrhosis of the liver.肝硬化腹水形成的病理生理学
Hepatogastroenterology. 1991 Oct;38(5):360-4.
2
Ascites in liver diseases.肝脏疾病中的腹水
Ann Ital Med Int. 1991 Jan-Mar;6(1 Pt 2):148-55.
3
[Pathogenesis of sodium and water retention in cirrhosis of the liver].[肝硬化时钠水潴留的发病机制]
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Pathogenesis of sodium and water retention in liver disease.肝脏疾病中钠和水潴留的发病机制。
Prog Liver Dis. 1992;10:329-47.
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Pathophysiology of ascites formation.
Gastroenterol Clin North Am. 1992 Mar;21(1):215-35.
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[Renal and extra-renal mechanisms of sodium and water retention in cirrhosis with ascites].[肝硬化腹水时钠水潴留的肾脏及肾外机制]
Rev Invest Clin. 1995 Jan-Feb;47(1):63-79.
8
Fluid retention in cirrhosis: pathophysiology and management.肝硬化中的液体潴留:病理生理学与管理
QJM. 2008 Feb;101(2):71-85. doi: 10.1093/qjmed/hcm121. Epub 2008 Jan 9.
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Pathogenetic factors and clinical elements in ascites and hepatorenal syndrome during liver cirrhosis.肝硬化腹水及肝肾综合征的发病因素与临床要素
Ann Ital Med Int. 1999 Oct-Dec;14(4):264-84.
10
Renal sodium retention and ascites formation in dogs with experimental cirrhosis but without portal hypertension or increased splanchnic vascular capacity.实验性肝硬化但无门静脉高压或内脏血管容量增加的犬的肾钠潴留和腹水形成
J Lab Clin Med. 1978 Mar;91(3):520-36.

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Renal sodium handling and neurohumoral systems in patients with cirrhosis in sitting posture: effects of spironolactone and water immersion.
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Clin Investig. 1993 Nov;71(11):894-7. doi: 10.1007/BF00185599.