Campbell V, Greig P D, Cranford J, Langer B, Silverman M, Blendis L M
Hepatology. 1982 Jan-Feb;2(1):54-8. doi: 10.1002/hep.1840020109.
To define the relationship between portal hypertension and renal excretion of salt and water, two acute animal models of portal hypertension were investigated. In both models, it was necessary for systemic and renal hemodynamics to remain unchanged during the creation of portal hypertension so as to eliminate the effects of change in these parameters on renal excretion. In eight dogs, portal hypertension was induced by controlled tightening of a ligature around the superior hepatic vein and changes in hemodynamics were prevented by controlled i.v. titration with canine plasma. Rises in portal pressure 9.3 +/- 2.6 to 15.6 +/- 2.3 cm H2O were associated with significant decreases in urine volume 1.57 +/- 0.53 to 0.66 +/- 0.21 ml per min (p less than 0.05) and urinary sodium excretion [340 +/- 82 to 145 +/- 75 mEq per min (p less than 0.05)]. In contrast, similar experiments in five dogs in which the portal vein was partially ligated with increases in portal pressure from 8.3 +/- 0.6 to 18.6 +/- 0.5 cm H2O resulted in no change in urinary volume or sodium excretion. Acute reversible portal hypertension induced by hepatic vein constriction is associated with acute reversible retention of water and salt in the absence of changes in renal blood flow and creatinine clearance which only occur when the liver is involved and not with portal vein constriction.
为了明确门静脉高压与肾盐和水排泄之间的关系，研究了两种急性门静脉高压动物模型。在这两种模型中，门静脉高压形成过程中全身和肾脏血流动力学必须保持不变，以消除这些参数变化对肾脏排泄的影响。在8只犬中，通过控制收紧肝上静脉周围的结扎线诱导门静脉高压，并通过静脉滴注犬血浆来防止血流动力学变化。门静脉压力从9.3±2.6厘米水柱升高至15.6±2.3厘米水柱，同时尿量从每分钟1.57±0.53毫升显著减少至0.66±0.21毫升（p<0.05），尿钠排泄从每分钟340±82毫当量减少至145±75毫当量（p<0.05）。相比之下，在5只犬中进行的类似实验，通过部分结扎门静脉使门静脉压力从8.3±0.6厘米水柱升高至18.6±0.5厘米水柱，尿量和钠排泄没有变化。肝静脉收缩诱导的急性可逆性门静脉高压与水和盐的急性可逆性潴留相关，而肾脏血流和肌酐清除率没有变化，后者仅在肝脏受累时发生，门静脉收缩时则不会发生。
