Vasodilatation and sodium retention in prehepatic portal hypertension

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 < 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 < 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.