Kalambokis Georgios, Economou Michalis, Kosta Paraskevi, Papadimitriou Konstantinos, Tsianos Epameinondas V
Department of Internal Medicine, Medical School of Ioannina, 45110 Ioannina, Greece.
J Clin Gastroenterol. 2006 Apr;40(4):342-6. doi: 10.1097/01.mcg.0000210101.74618.61.
To evaluate the effects of diuretic treatment, octreotide, or both on portal hemodynamics in nonazotemic cirrhotic patients with ascites.
Diuretics and octreotide have been associated with a decrease in portal pressure in cirrhotic patients, suggested to be mediated by plasma volume depletion and splanchnic vasoconstriction, respectively. However, liver cirrhosis is characterized by activation of the renin-angiotensin-aldosterone axis, which increases hepatic vascular resistance and is augmented or suppressed by diuretics or octreotide, respectively.
Twenty nonazotemic cirrhotic patients with ascites were treated with furosemide and spironolactone. Of them, 10 (group 1) discontinued diuretic treatment for 7 days. Thereafter for 5 days, each patient received subcutaneous octreotide, 300 microg twice per day; ten of them (group 2) received the octreotide in addition to their usual diuretic treatment. Portal and systemic hemodynamics with Doppler ultrasound and endogenous vasoactive systems were evaluated while the patients received diuretics (both groups), after discontinuation of diuretics (group 1), and after octreotide administration (both groups).
The withdrawal of diuretics did not alter portal hemodynamics, but it impaired systemic hemodynamics and suppressed the renin-aldosterone axis. The addition of octreotide to diuretic treatment but not octreotide alone improved portal and systemic hemodynamics. In both groups the initiation of octreotide administration suppressed the renin-aldosterone axis and plasma glucagon levels.
In nonazotemic cirrhotic patients with ascites, the combination of diuretics and octreotide improves systemic hemodynamics and inhibits the diuretic-related component of the activated renin-aldosterone axis, which in turn augments the portal hypotensive effect of diuretic-induced plasma volume depletion.
评估利尿剂治疗、奥曲肽或两者联用对非氮质血症性肝硬化腹水患者门静脉血流动力学的影响。
利尿剂和奥曲肽与肝硬化患者门静脉压力降低有关，分别提示是由血浆容量减少和内脏血管收缩介导的。然而，肝硬化的特征是肾素 - 血管紧张素 - 醛固酮轴激活，这会增加肝血管阻力，且分别被利尿剂或奥曲肽增强或抑制。
20例非氮质血症性肝硬化腹水患者接受呋塞米和螺内酯治疗。其中10例（第1组）停用利尿剂治疗7天。此后5天，每位患者每天两次皮下注射300微克奥曲肽；其中10例（第2组）在常规利尿剂治疗基础上加用奥曲肽。在患者接受利尿剂治疗时（两组）、停用利尿剂后（第1组）以及奥曲肽给药后（两组），用多普勒超声评估门静脉和全身血流动力学以及内源性血管活性系统。
停用利尿剂未改变门静脉血流动力学，但损害了全身血流动力学并抑制了肾素 - 醛固酮轴。利尿剂治疗加用奥曲肽而非单独使用奥曲肽改善了门静脉和全身血流动力学。两组中奥曲肽给药均抑制了肾素 - 醛固酮轴和血浆胰高血糖素水平。
在非氮质血症性肝硬化腹水患者中，利尿剂和奥曲肽联用可改善全身血流动力学，并抑制激活的肾素 - 醛固酮轴中与利尿剂相关的成分，这反过来增强了利尿剂诱导的血浆容量减少的门静脉降压作用。
