Putensen C, Hörmann C, Kleinsasser A, Putensen-Himmer G
Division of Intensive Care Medicine, Department of Anesthesia and Intensive Care Medicine, University of Innsbruck, Innsbruck, Austria.
Am J Respir Crit Care Med. 1998 Jun;157(6 Pt 1):1743-7. doi: 10.1164/ajrccm.157.6.9609017.
Ten patients with acute respiratory distress syndrome (ARDS) received in random order nitric oxide (NO) inhalation, aerosolized prostaglandin E1 (PGE1), infusion of PGE1, or no intervention. Inhalation of either aerosolized PGE1 (10 +/- 1 ng/kg/min) or NO (7 +/- 1 ppm) reduced pulmonary vascular resistance (PVR) from 158 +/- 14 to 95 +/- 11 dyn . s/cm5/m2 (NO) and 100 +/- 12 dyn . s/cm5/m2 (aerosolized PGE1), and improved PaO2 from 78 +/- 3 to 96 +/- 5 mm Hg (NO) and 95 +/- 4 mm Hg (aerosolized PGE1) (p < 0.05), venous admixture (Q VA/Q T) from 45 +/- 2 to 36 +/- 2% (NO), and 36 +/- 2% (aerosolized PGE1) (p < 0.05), oxygen delivery (DO2) from 711 +/- 34 to 762 +/- 45 ml/min/m2 (NO) and 780 +/- 46 ml/min/m2 (aerosolized PGE1) (p < 0.05), and right ventricular ejection fraction (RVEF) from 32 +/- 6 to 37 +/- 5% (NO), and 36 +/- 4% (aerosolized PGE1) (p < 0.05) at a constant cardiac index (CI). Although infusion of PGE1 (12 +/- 1 ng/kg/min) caused a similar reduction in PVR as aerosolized PGE1 and NO inhalation, it improved RVEF and increased CI but decreased Q VA/Q T and PaO2. These results suggest that in ARDS patients inhalation of aerosolized PGE1 or NO in low concentrations equally improves PVR and gas exchange by selective vasodilation in ventilated areas.
十名急性呼吸窘迫综合征（ARDS）患者被随机安排接受一氧化氮（NO）吸入、雾化前列腺素E1（PGE1）、静脉输注PGE1或不进行干预。雾化PGE1（10±1 ng/kg/分钟）或NO（7±1 ppm）吸入均使肺血管阻力（PVR）从158±14降至95±11达因·秒/厘米⁵/平方米（NO）和100±12达因·秒/厘米⁵/平方米（雾化PGE1），并使动脉血氧分压（PaO2）从78±3升至96±5毫米汞柱（NO）和95±4毫米汞柱（雾化PGE1）（p<0.05），静脉血掺杂（Q VA/Q T）从45±2降至36±2%（NO）和36±2%（雾化PGE1）（p<0.05），氧输送（DO2）从711±34升至762±45毫升/分钟/平方米（NO）和780±46毫升/分钟/平方米（雾化PGE1）（p<0.05），右心室射血分数（RVEF）从32±6升至37±5%（NO）和36±4%（雾化PGE1）（p<0.05），且心指数（CI）恒定。虽然静脉输注PGE1（12±1 ng/kg/分钟）导致的PVR降低与雾化PGE1和NO吸入相似，但它改善了RVEF并增加了CI，但降低了Q VA/Q T和PaO2。这些结果表明，在ARDS患者中，低浓度雾化PGE1或NO吸入通过在通气区域选择性血管舒张同样改善了PVR和气体交换。
