PERIPHERAL ARTERIAL VASODILATION HYPOTHESIS - A PROPOSAL FOR THE INITIATION OF RENAL SODIUM AND WATER-RETENTION IN CIRRHOSIS
PERIPHERAL ARTERIAL VASODILATION HYPOTHESIS - A PROPOSAL FOR THE INITIATION OF RENAL SODIUM AND WATER-RETENTION IN CIRRHOSIS
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DOI：
10.1002/hep.1840080532
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发表时间：
1988-09-01
期刊：
影响因子：
13.5
通讯作者：
RODES, J
中科院分区：
文献类型：
--
作者：
SCHRIER, RW;ARROYO, V;RODES, J
在实验性肝硬化中，肾脏钠和水潴留和血浆容量扩张已被证明先于腹水形成。经典的“欠充”理论，即腹水的形成导致低血容量并引发继发性肾钠和水潴留，因此似乎不太可能。虽然原发性肾钠和水潴留以及腹水形成前血浆容量扩张的发生有利于“溢出”假说，但与肝硬化相关的肾素-血管紧张素-醛固酮系统、血管加压素释放和交感神经系统的刺激与原发性容量扩张不一致。在这篇文章中，“外周动脉血管舒张假说”被认为是肝硬化中钠和水潴留的发起者。外周动脉血管舒张是肝硬化患者和肝硬化实验动物最早观察到的现象之一。动脉血管扩张和动静脉瘘是继发于动脉血管树充盈减少的肾钠和水潴留的其他例子。心输出量增加和激素刺激是肝硬化、动静脉瘘和药物引起的外周动脉血管扩张的共同特征。然而，由于门静脉高压的存在，保留的钠和水更容易渗入腹腔。外周动脉血管舒张假说也解释了从代偿性肝硬化到失代偿性肝硬化再到肝肾综合征的连续性。
Renal sodium and water retention and plasma volume expansion have been shown to precede ascites formation in experimental cirrhosis. The classical "underfilling" theory, in which ascites formation causes hypovolemia and initiates secondary renal sodium and water retention, thus seems unlikely. While the occurrence of primary renal sodium and water retention and plasma volume expansion prior to ascites formation favors the "overflow" hypothesis, the stimulation of the renin-angiotensin-aldosterone system, vasopressin release and sympathetic nervous system associated with cirrhosis is not consonant with primary volume expansion. In this present article, the "Peripheral Arterial Vasodilation Hypothesis" is proposed as the initiator of sodium and water retention in cirrhosis. Peripheral arterial vasodilation is one of the earliest observations in the cirrhotic patient and experimental animals with cirrhosis. Arterial vasodilators and arteriovenous fistula are other examples in which renal sodium and water retention occur secondary to a decreased filling of the arterial vascular tree. An increase in cardiac output and hormonal stimulation are common features of cirrhosis, arteriovenous fistula and drug-induced peripheral arterial vasodilation. However, a predilection for the retained sodium and water to transudate into the abdominal cavity occurs with cirrhosis because of the presence of portal hypertension. The Peripheral Arterial Vasodilation Hypothesis also explains the continuum from compensated to decompensated cirrhosis to the hepatorenal syndrome.