Albillos A, Colombato L A, Groszmann R J
Hepatic Hemodynamic Laboratory, Department of Veterans Affairs, Medical Center, West Haven, Connecticut.
Gastroenterology. 1992 Mar;102(3):931-5. doi: 10.1016/0016-5085(92)90179-3.
Sodium retention and peripheral vasodilatation are common consequences of portal hypertension secondary to cirrhosis. Although peripheral vasodilatation has been extensively documented in prehepatic portal hypertension, it is not known whether sodium retention is also a feature of this entity. The aim of this study in portal vein-constricted rats was to evaluate (a) whether sodium retention is a feature of prehepatic portal hypertension and (b) if sodium retention is present in this model, what its temporal relationship with peripheral vasodilatation might be. It was proposed that an understanding of the temporal interplay between peripheral vasodilatation and sodium retention could shed light on the current theories of sodium retention in portal hypertension. Rats were studied 1, 2, 3, and 4 days after partial portal vein ligation (n = 80) or sham operation (n = 63). Sodium retention was evaluated by changes in the size of the sodium space measured by the volume of distribution of 22Na. Systemic vascular resistance was calculated from mean arterial pressure (measured by arterial catheterization) and cardiac index (measured by thermodilution). A decrease in systemic vascular resistance was already observed on day 1 after constriction of the portal vein (4.2 +/- 0.2 vs. 5.2 +/- 6.1 mm Hg.min.mL-1.100 g; P less than 0.01). However, an expansion of the sodium space, which indicates sodium retention, was not observed until day 2 after induction of portal hypertension (37.1 +/- 0.8 vs. 32.6 +/- 0.7 mL.100 g-1; P less than 0.01). Therefore, sodium retention should be considered along with peripheral vasodilatation among the characteristic features of prehepatic portal hypertension. Because the reduction in systemic vascular resistance preceded the expansion of the sodium space by at least 24 hours, the finding of this study indicates that sodium retention follows peripheral vasodilatation.
钠潴留和外周血管扩张是肝硬化继发门静脉高压的常见后果。尽管外周血管扩张在肝前性门静脉高压中已有广泛记载，但尚不清楚钠潴留是否也是该病症的一个特征。本研究旨在评估门静脉缩窄大鼠模型中：(a) 钠潴留是否为肝前性门静脉高压的一个特征；(b) 如果该模型中存在钠潴留，那么它与外周血管扩张的时间关系是怎样的。有人提出，了解外周血管扩张和钠潴留之间的时间相互作用可能有助于阐明当前门静脉高压钠潴留理论。对部分门静脉结扎术后1、2、3和4天的大鼠（n = 80）或假手术大鼠（n = 63）进行研究。通过用22Na分布容积测量钠空间大小的变化来评估钠潴留情况。根据平均动脉压（通过动脉插管测量）和心指数（通过热稀释测量）计算全身血管阻力。门静脉缩窄后第1天即已观察到全身血管阻力降低（4.2±0.2 vs. 5.2±6.1 mmHg·min·mL-1·100 g；P < 0.01）。然而，直到门静脉高压诱导后第2天才观察到表明钠潴留的钠空间扩大（37.1±0.8 vs. 32.6±0.7 mL·100 g-1；P < 0.01）。因此，钠潴留应与外周血管扩张一并被视为肝前性门静脉高压的特征。由于全身血管阻力降低比钠空间扩大至少提前24小时出现，本研究结果表明钠潴留发生在外周血管扩张之后。
