Gadano A, Moreau R, Vachiery F, Soupison T, Yang S, Cailmail S, Sogni P, Hadengue A, Durand F, Valla D, Lebrec D
Laboratoire d'Hémodynamique Splanchnique, Unité de Recherches de Physiopathologie Hépatique, INSERM U-24, Hôpital Beaujon, Clichy, France.
J Hepatol. 1997 Jun;26(6):1229-34. doi: 10.1016/s0168-8278(97)80456-4.
BACKGROUND/AIMS: Refractory ascites, which occurs in certain patients with cirrhosis, is associated with a blunted natriuretic response to exogenous atrial natriuretic peptide (ANP). Since this blunting seems to be related to ANP-induced arterial hypotension, a vasoconstrictor, such as terlipressin (a vasopressin analogue), may restore natriuresis to exogenous ANP. Moreover, since cirrhosis-elicited vasodilation is thought to play a role in sodium retention, a vasoconstriction caused by terlipressin alone may lead to an increase in sodium excretion. This study aimed to evaluate the natriuretic response to either a combination of ANP with terlipressin or terlipressin alone in patients with cirrhosis and refractory ascites.
Sixteen consecutive patients with cirrhosis and refractory ascites were randomly assigned to receive either a combination of terlipressin (1-2 mg, i.v. bolus) with ANP (35 ng/kg, i.v. bolus followed by 15 ng x kg(-1) x min(-1) for 60 min) (n=8) or terlipressin alone (1-2 mg, i.v. bolus) (n=8). Sodium excretion and urine output, systemic, splanchnic and renal hemodynamics and renal oxygen consumption were measured before and during treatments.
Combined therapy did not change arterial pressure but significantly increased urinary sodium excretion and urine output. These effects were associated with a significant increase in glomerular filtration rate and a decrease in renal oxygen consumption. Terlipressin alone significantly increased arterial pressure but did not change urinary sodium excretion or urine output. Moreover, terlipressin did not change either glomerular filtration rate or renal oxygen consumption.
The combination of exogenous ANP with terlipressin, but not terlipressin alone, increases sodium excretion in patients with cirrhosis and refractory ascites.
背景/目的：难治性腹水发生于某些肝硬化患者，与外源性心房利钠肽（ANP）引起的利钠反应减弱有关。由于这种减弱似乎与ANP诱导的动脉低血压有关，一种血管收缩剂，如特利加压素（一种加压素类似物），可能会恢复外源性ANP的利钠作用。此外，由于肝硬化引起的血管舒张被认为在钠潴留中起作用，单独由特利加压素引起的血管收缩可能导致钠排泄增加。本研究旨在评估肝硬化和难治性腹水患者对ANP与特利加压素联合使用或单独使用特利加压素的利钠反应。
16例连续的肝硬化和难治性腹水患者被随机分配接受特利加压素（1 - 2mg，静脉推注）与ANP（35ng/kg，静脉推注，随后以15ng·kg⁻¹·min⁻¹持续60分钟）联合治疗（n = 8）或单独使用特利加压素（1 - 2mg，静脉推注）（n = 8）。在治疗前和治疗期间测量钠排泄和尿量、全身、内脏和肾脏血流动力学以及肾脏氧消耗。
联合治疗未改变动脉压，但显著增加尿钠排泄和尿量。这些效应与肾小球滤过率显著增加和肾脏氧消耗减少有关。单独使用特利加压素显著增加动脉压，但未改变尿钠排泄或尿量。此外，特利加压素未改变肾小球滤过率或肾脏氧消耗。
外源性ANP与特利加压素联合使用而非单独使用特利加压素可增加肝硬化和难治性腹水患者的钠排泄。
