Hadengue A, Moreau R, Bacq Y, Gaudin C, Braillon A, Lebrec D
Unité de Recherches de Physiopathologie Hépatique (INSERM U 24), Hôpital Beaujon, France.
Hepatology. 1991 Jan;13(1):111-6.
We studied the effects of fenoldopam, a selective dopamine DA1 agonist on systemic and splanchnic hemodynamics, renal blood flow and sodium excretion in 12 patients with alcoholic cirrhosis and ascites. Hepatic, azygos and renal veins were catheterized before and after intravenous administration of fenoldopam, 0.05 micrograms/kg/min for 1 hr and increased to 0.1 micrograms/kg/min for another hour. Mean arterial pressure progressively decreased (from 83 +/- 7 to a minimum of 77 +/- 8 mm Hg 100 min after starting the infusion) but returned to baseline level at 120 min. Plasma norepinephrine and renin activity increased (respectively from 567 +/- 297 to 919 +/- 375 pg/ml, p less than 0.05, and from 17 +/- 14 to 23 +/- 15 ng/ml/hr, p less than 0.05). Renal blood flow, urine output or sodium excretion did not change. Sodium output decreased at 1 hr from 6.9 mumol/min to 4.0 mumol/min, p less than 0.05. Both hepatic venous pressure gradient and azygos blood flow significantly increased by 21%. We conclude that the acute administration of fenoldopam did not improve renal hemodynamics or function in patients with cirrhosis and ascites. In addition, dopamine DA1 agonism caused further increases in norepinephrine concentration and plasma renin activity. Portal pressure also increased, probably because of an increase in mesenteric blood flow. These results question the renal benefit and raise concern about the use of dopamine agonists in patients with cirrhosis and ascites.
我们研究了选择性多巴胺DA1激动剂非诺多泮对12例酒精性肝硬化腹水患者全身和内脏血流动力学、肾血流量及钠排泄的影响。在静脉输注非诺多泮前及输注过程中,经导管分别测定肝静脉、奇静脉和肾静脉的血流动力学参数。非诺多泮以0.05微克/千克/分钟的速度静脉输注1小时,随后增加至0.1微克/千克/分钟,再输注1小时。平均动脉压逐渐下降(从83±7毫米汞柱降至输注开始后100分钟时的最低值77±8毫米汞柱),但在120分钟时恢复至基线水平。血浆去甲肾上腺素和肾素活性升高(分别从567±297皮克/毫升升至919±375皮克/毫升,P<0.05;从17±14纳克/毫升/小时升至23±15纳克/毫升/小时,P<0.05)。肾血流量、尿量或钠排泄量未发生变化。钠排泄量在1小时时从6.9微摩尔/分钟降至4.0微摩尔/分钟,P<0.05。肝静脉压力梯度和奇静脉血流量均显著增加21%。我们得出结论,急性给予非诺多泮并不能改善肝硬化腹水患者的肾血流动力学或功能。此外,多巴胺DA1激动作用导致去甲肾上腺素浓度和血浆肾素活性进一步升高。门静脉压力也升高,可能是由于肠系膜血流量增加所致。这些结果对使用多巴胺激动剂给肝硬化腹水患者带来的肾脏益处提出质疑,并引发了人们对其使用的担忧。