Schenk P, Madl C, Rezaie-Majd S, Lehr S, Müller C
Department of Internal Medicine 4, Intensive Care, University of Vienna, Allgemeines Krankenhaus, Waehringer Guertel 18-20, A-1090 Vienna, Austria.
Ann Intern Med. 2000 Nov 7;133(9):701-6. doi: 10.7326/0003-4819-133-9-200011070-00012.
The hypoxemia of the hepatopulmonary syndrome, seen in patients with severe chronic liver dysfunction, results from widespread pulmonary vasodilation. No established drug therapy is available for this condition.
To study the effect of methylene blue, a potent inhibitor of guanylate cyclase, in patients with severe hepatopulmonary syndrome.
Open, uncontrolled trial.
Medical intensive care unit at the university hospital in Vienna, Austria.
7 patients with advanced cirrhosis and severe hepatopulmonary syndrome with PaO(2) of 60 mm Hg or less.
Insertion of a pulmonary artery catheter and an arterial indwelling catheter; intravenous administration of methylene blue, 3 mg/kg of body weight, over a 15-minute period.
Serial measurements of gas exchange and hemodynamic variables.
After methylene blue administration, PaO(2) increased in all patients (from a baseline mean +/- SD of 58 +/- 2.5 mm Hg to 74 +/- 11.5 mm Hg 5 hours after infusion; P = 0.006) and the alveolar-arterial difference for partial pressure of oxygen (PAO(2) - PaO(2) ) decreased in all patients, with a maximum effect achieved after 5 hours (from 49 +/- 3.3 mm Hg to 30 +/- 10.4 mm Hg; P = 0.003); even after 10 hours, PAO(2) - PaO(2) was still significantly reduced compared with baseline (P = 0.041). Oxygenation improved because of reduction in shunt fraction (from 41% +/- 3.1% to 25% +/- 4.5%; P < 0.001). Mean pulmonary artery pressure increased (from 20 +/- 5.2 mm Hg to 23 +/- 3.6 mm Hg; P = 0. 028), as did pulmonary vascular resistance (from 58 +/- 23 dyne/sec. cm(-5) to 115 +/- 56 dyne/sec. cm(-5); P = 0.012). Arterial blood pressure did not change significantly. Cardiac output decreased (from 10.6 +/- 2.2 L/min to 8.6 +/- 2.7 L/min; P = 0.008) and systemic vascular resistance increased (from 527 +/- 144 dyne/sec. cm(-5) to 729 +/- 222 dyne/sec. cm(-5); P = 0.037). Heart rate, central venous pressure, and pulmonary capillary wedge pressure remained unchanged.
Intravenous methylene blue improved hypoxemia and hyperdynamic circulation in patients with liver cirrhosis and severe hepatopulmonary syndrome.
严重慢性肝功能不全患者出现的肝肺综合征低氧血症是由广泛的肺血管扩张所致。目前尚无针对该病症的确立药物疗法。
研究鸟苷酸环化酶强效抑制剂亚甲蓝对严重肝肺综合征患者的疗效。
开放、非对照试验。
奥地利维也纳大学医院的医学重症监护病房。
7例晚期肝硬化且严重肝肺综合征患者，其动脉血氧分压（PaO₂）≤60 mmHg。
插入肺动脉导管和动脉留置导管；在15分钟内静脉注射亚甲蓝，剂量为3 mg/kg体重。
连续测量气体交换和血流动力学变量。
注射亚甲蓝后，所有患者的PaO₂均升高（从基线时的平均±标准差58±2.5 mmHg升至输注后5小时的74±11.5 mmHg；P = 0.006），所有患者的氧分压肺泡 - 动脉差（PAO₂ - PaO₂）均降低，5小时时达到最大效应（从49±3.3 mmHg降至30±10.4 mmHg；P = 0.003）；即使在10小时后，PAO₂ - PaO₂仍较基线显著降低（P = 0.041）。由于分流分数降低（从41%±3.1%降至25%±4.5%；P < 0.001），氧合得到改善。平均肺动脉压升高（从20±5.2 mmHg升至23±3.6 mmHg；P = 0.028），肺血管阻力也升高（从58±23达因/秒·厘米⁻⁵升至115±56达因/秒·厘米⁻⁵；P = 0.012）。动脉血压无显著变化。心输出量降低（从10.6±2.2升/分钟降至8.6±2.7升/分钟；P = 0.008），全身血管阻力升高（从527±144达因/秒·厘米⁻⁵升至729±222达因/秒·厘米⁻⁵；P = 0.037）。心率、中心静脉压和肺毛细血管楔压保持不变。
静脉注射亚甲蓝可改善肝硬化和严重肝肺综合征患者的低氧血症和高动力循环状态。
