Murakami S, Ohno T, Bernardo J F, Pfeifer C A, Li T, Zhang Y, Dubey R K, Branch R A, Sabra R
Center for Clinical Pharmacology, University of Pittsburgh Medical Center, Pennsylvania 15213-2582, USA.
J Gastroenterol Hepatol. 1996 Sep;11(9):850-6. doi: 10.1111/j.1440-1746.1996.tb00092.x.
Sodium retention along with peripheral vasodilation are features of prehepatic portal hypertension. In several models of experimental liver damage, sodium retention occurs only when hepatic function, measured by the aminopyrine breath test (ABT-k), falls below a critical threshold. The relationship between renal sodium handling, ABT-k and systemic and renal haemodynamics in partial portal vein ligated (PVL) rats was examined to test hypothesis that peripheral vasodilation was responsible for initiating sodium retention. Haemodynamic measurements were conducted early after surgery in portal hypertensive rats with and without sodium retention and in sham-operated controls. Compared with control, both PVL groups of rats had elevated portal pressure and lower peripheral vascular resistance (P < 0.05). Sodium retaining-PVL rats had both lower ABT-k (0.95 +/- 0.05 vs 1.38 +/- 0.06 x 10(-2)/min; P < 0.05) and higher sodium balance (1.38 +/- 0.09 vs 0.43 +/- 0.09 mmol/day; P < 0.05) than non-sodium retaining PVL rats. No differences in plasma renin activity or noradrenaline concentrations were observed. In a separate group of rats, hydralazine-induced pheripheral vasodilation did not induce sodium retention. These results suggest that the presence of peripheral vasodilation alone is not sufficient to trigger a sodium-retaining status. A factor, probably liver function-dependent, acting directly on renal tubules may be necessary for changes in renal sodium handling in this model.
钠潴留以及外周血管舒张是肝前门静脉高压的特征。在几种实验性肝损伤模型中，只有当通过氨基比林呼吸试验（ABT-k）测得的肝功能降至临界阈值以下时，才会发生钠潴留。研究了部分门静脉结扎（PVL）大鼠肾钠处理、ABT-k与全身及肾血流动力学之间的关系，以检验外周血管舒张引发钠潴留这一假说。对术后早期有或无钠潴留的门静脉高压大鼠以及假手术对照组进行了血流动力学测量。与对照组相比，两组PVL大鼠的门静脉压力均升高，外周血管阻力降低（P<0.05）。钠潴留的PVL大鼠的ABT-k较低（0.95±0.05对1.38±0.06×10⁻²/min；P<0.05），钠平衡较高（1.38±0.09对0.43±0.09 mmol/天；P<0.05），高于无钠潴留的PVL大鼠。未观察到血浆肾素活性或去甲肾上腺素浓度的差异。在另一组大鼠中，肼苯哒嗪诱导的外周血管舒张未引起钠潴留。这些结果表明，仅外周血管舒张的存在不足以引发钠潴留状态。在该模型中，可能依赖肝功能且直接作用于肾小管的一个因素对于肾钠处理的改变可能是必要的。
