Levy M, Maher E, Wexler M J
Department of Physiology, McGill University, Montréal, Qué., Canada.
Can J Physiol Pharmacol. 1988 Jan;66(1):80-3. doi: 10.1139/y88-015.
Dogs with chronic biliary cirrhosis and portal hypertension commonly develop plasma volume expansion, urinary sodium retention, ascites, and perturbed systemic hemodynamics, i.e., a rise in cardiac output and a fall in peripheral vascular resistance. Our laboratory has previously demonstrated that creating a side-side portacaval anastomosis in such animals, and so venting hepatoportal pressure, will prevent sodium retention and ascites formation and will maintain the animals euvolemic. In the present study, in four cirrhotic dogs with such an anastomosis, observations made at 12 weeks postbiliary duct ligation, and in the presence of grossly disturbed liver function and morphology, failed to demonstrate any change from control conditions in arterial blood pressure, cardiac output, or peripheral vascular resistance. We conclude that venting hepatoportal pressure in cirrhotic dogs with markedly disturbed liver function prevents the advent of a hyperdynamic circulation, possibly by preventing volume expansion.
患有慢性胆汁性肝硬化和门静脉高压的犬类通常会出现血容量扩张、尿钠潴留、腹水以及全身血流动力学紊乱，即心输出量增加和外周血管阻力降低。我们实验室之前已经证明，在此类动物中建立侧侧门腔静脉吻合术以释放肝门静脉压力，可防止钠潴留和腹水形成，并维持动物的血容量正常。在本研究中，对4只进行了这种吻合术的肝硬化犬进行观察，在胆管结扎12周后，且肝功能和形态严重受损的情况下，未发现动脉血压、心输出量或外周血管阻力与对照情况有任何变化。我们得出结论，在肝功能明显受损的肝硬化犬中释放肝门静脉压力可防止高动力循环的出现，可能是通过防止血容量扩张来实现的。
