Rojter S, Tessler J, Alvarez D, Persico R, Lopez P, Bandi J C, Podesta A, Terg R, Gutman R, Mastai R
Liver Section, Hospital Italiano, Buenos Aires, Argentina.
J Hepatol. 1995 Feb;22(2):184-8. doi: 10.1016/0168-8278(95)80427-7.
BACKGROUND/AIMS: An experimental study has shown that propylthiouracil increases portal blood flow in normal rats. Whether propylthiouracil has a similar effect in patients with alcoholic cirrhosis remains to be demonstrated. The aim of this study was to evaluate the effects of oral propylthiouracil (300 mg) on systemic and portal hemodynamics in patients with alcoholic cirrhosis.
Plasma propylthiouracil levels were also measured by high performance liquid chromatography in five patients with alcoholic cirrhosis. In eight patients with cirrhosis, mean arterial pressure, cardiac output and portal blood flow were evaluated before and after placebo and propylthiouracil administration. Hemodynamic measurements were performed by the Doppler technique. The plasma peak level of propylthiouracil was achieved at 1.4 +/- 0.1 h in patients with alcoholic cirrhosis. This time was chosen to express hemodynamic changes.
Propylthiouracil administration caused a significant increase in portal blood flow (+16.5%, p < 0.05) in patients with alcoholic cirrhosis. This effect was associated with a mild and significant rise in cardiac output (from 5.8 +/- 0.2 to 6.1 +/- 0.3 l/min, p < 0.05) and a decrease in peripheral vascular resistance (from 1171 +/- 69 to 1070 +/- 67 dyn . s-1 . cm-5, p < 0.01). A significant correlation was observed between changes in portal blood flow and peripheral vascular resistance (r = 0.79, p < 0.05). No significant changes were observed after placebo.
Our findings show that propylthiouracil has a vasodilatory effect in patients with alcoholic cirrhosis. We postulate that this effect could be the mechanism by which propylthiouracil decreases hypermetabolic state, and increases oxygen delivery to the liver, in patients with alcoholic liver diseases.
背景/目的：一项实验研究表明，丙硫氧嘧啶可增加正常大鼠的门静脉血流量。丙硫氧嘧啶在酒精性肝硬化患者中是否有类似作用仍有待证实。本研究的目的是评估口服丙硫氧嘧啶（300毫克）对酒精性肝硬化患者全身和门静脉血流动力学的影响。
还通过高效液相色谱法测量了5例酒精性肝硬化患者的血浆丙硫氧嘧啶水平。对8例肝硬化患者在服用安慰剂和丙硫氧嘧啶前后评估平均动脉压、心输出量和门静脉血流量。采用多普勒技术进行血流动力学测量。酒精性肝硬化患者丙硫氧嘧啶的血浆峰值水平在1.4±0.1小时达到。选择这个时间来表示血流动力学变化。
丙硫氧嘧啶给药使酒精性肝硬化患者的门静脉血流量显著增加（+16.5%，p<0.05）。这种作用与心输出量轻度但显著增加（从5.8±0.2升/分钟增加到6.1±0.3升/分钟，p<0.05）和外周血管阻力降低（从1171±69降至1070±67达因·秒-1·厘米-5，p<0.01）有关。门静脉血流量变化与外周血管阻力之间存在显著相关性（r=0.79，p<0.05）。服用安慰剂后未观察到显著变化。
我们的研究结果表明，丙硫氧嘧啶对酒精性肝硬化患者有血管舒张作用。我们推测，这种作用可能是丙硫氧嘧啶降低酒精性肝病患者高代谢状态并增加肝脏氧输送的机制。
