Zwissler B, Kemming G, Habler O, Kleen M, Merkel M, Haller M, Briegel J, Welte M, Peter K
Department of Anesthesiology, Ludwig-Maximilians-Universität München, Germany.
Am J Respir Crit Care Med. 1996 Dec;154(6 Pt 1):1671-7. doi: 10.1164/ajrccm.154.6.8970353.
Inhalation of nitric oxide (NO) and prostacyclin (PGI2) may induce selective pulmonary vasodilation and-by improving ventilation-perfusion ratio in ventilated areas of the lung-increase Pao2 in patients with acute lung injury. To assess the therapeutic efficacy of both compounds, dose-response curves were established in patients with adult respiratory distress syndrome (ARDS). Patients received both PGI2 (doses of 1, 10, and 25 ng/kg/min) and NO (concentrations of 1, 4, and 8 ppm). Cardiorespiratory parameters were assessed at control, at each drug concentration, and after withdrawal of NO and PGI2. PGI2 resulted in a significant, dose-dependent and selective reduction of pulmonary artery pressure (PAP) from 35.1 +/- 6.3 mm Hg at control to 33.1 +/- 4.8 (1 ng/kg/min), 31.3 +/- 4.8 mm Hg (10 ng/kg/min) and 29.6 +/- 4.5 mm Hg (25 ng/kg/min), respectively. Inhaled NO reduced PAP from 34.5 +/- 5.6 to 32.1 +/- 5.9 mm Hg at 4 ppm, and to 31.8 +/- 6.1 mm Hg at 8 ppm, respectively, with no effect at 1 ppm. Pao2/Flo2 ratio increased from 105 +/- 37 to 125 +/- 56 mm Hg (range of increase: 0 to 57 mm Hg) at PGI2 10 ng/kg/min and to 131 +/- 63 mm Hg (range: -5 to 89 mm Hg) at 25 ng/kg/min with no effect at 1 ng/kg/min. NO improved Pao2 (e.g., from 116 +/- 47 to 167 +/- 86 mm Hg at 8 ppm) and reduced intrapulmonary shunt at all doses tested. We conclude that both inhaled PGI2 and NO may induce selective pulmonary vasodilation and increase Pao2 in severe ARDS.
吸入一氧化氮（NO）和前列环素（PGI2）可诱导选择性肺血管舒张，并通过改善肺通气区域的通气/灌注比，提高急性肺损伤患者的动脉血氧分压（Pao2）。为评估这两种化合物的治疗效果，对成人呼吸窘迫综合征（ARDS）患者建立了剂量-反应曲线。患者分别接受PGI2（剂量为1、10和25 ng/kg/分钟）和NO（浓度为1、4和8 ppm）。在对照状态、每个药物浓度时以及停用NO和PGI2后评估心肺参数。PGI2导致肺动脉压（PAP）显著、剂量依赖性且选择性降低，从对照时的35.1±6.3 mmHg分别降至33.1±4.8（1 ng/kg/分钟）、31.3±4.8 mmHg（10 ng/kg/分钟）和29.6±4.5 mmHg（25 ng/kg/分钟）。吸入NO使PAP在4 ppm时从34.5±5.6降至32.1±5.9 mmHg，在8 ppm时降至31.8±6.1 mmHg，在1 ppm时无影响。在PGI2为10 ng/kg/分钟时，Pao2/Flo2比值从105±37升至125±56 mmHg（升高范围：0至57 mmHg），在25 ng/kg/分钟时升至131±63 mmHg（范围：-5至89 mmHg），在1 ng/kg/分钟时无影响。在所有测试剂量下，NO均改善了Pao2（例如，在8 ppm时从116±47升至167±86 mmHg）并减少了肺内分流。我们得出结论，吸入PGI2和NO均可诱导选择性肺血管舒张并提高重症ARDS患者的Pao2。
