Gommers D, Hartog A, van 't Veen A, Lachmann B
Department of Anesthesiology, Erasmus University Rotterdam, The Netherlands.
Crit Care Med. 1997 Nov;25(11):1868-73. doi: 10.1097/00003246-199711000-00027.
The inhalation of nitric oxide increases oxygenation by improving the ventilation/perfusion ratios in neonates with respiratory distress syndrome and those ratios in adults with acute respiratory distress syndrome. There is evidence that inhaled nitric oxide is ineffective when the lung remains atelectatic and poorly inflated. This study aimed to enhance nitric oxide delivery by improving lung aeration by means of exogenous surfactant or by increasing positive end-expiratory pressure.
Experimental, comparative study.
Research laboratory of a large university.
Twenty-eight adult New Zealand white rabbits, weighing 2.7 +/- 0.3 kg.
Lung injury was induced by repeated whole-lung lavage with saline. The animals were mechanically ventilated with a tidal volume of 10 mL/kg, an FIO2 of 1.0, and a positive end-expiratory pressure of 6 cm H2O. Forty-five minutes after the last lavage, the animals were randomly assigned to five groups. In two groups, lung aeration was first increased either by instillation of a low dose of exogenous surfactant (25 mg/kg) or by increasing the positive end-expiratory pressure to 10 cm H2O, before inhalation of nitric oxide was started. In each of these animals, five different nitric oxide concentrations (4 to 20 parts per million) were inhaled for 30 mins, followed by a 30-min washout period. The other three groups served as controls and received only one treatment protocol: nitric oxide (4 to 20 parts per million), or surfactant (25 mg/kg), or positive end-expiratory pressure (10 cm H2O).
Before and after lavage, blood gases and lung mechanics were measured every 30 mins. Both strategies to increase lung aeration improved PaO2 values from 61 +/- 13 torr (8.1 +/- 1.7 kPa) to 200 to 300 torr (26.6 to 39.9 kPa) in 30 mins. After inhalation of nitric oxide, additional increases of oxygenation were seen only in the animals that received a low dose (25 mg/kg) of surfactant. The control group that inhaled nitric oxide showed no significant change in oxygenation, and four of the six animals did not survive the observation period. In the two groups in which positive end-expiratory pressure was increased to 10 cm H2O, half of the animals developed a pneumothorax during the observation period.
These data indicate that inhaled nitric oxide is able to improve arterial oxygenation after alveolar recruitment by means of a low dose of exogenous surfactant, and not by increase of positive end-expiratory pressure from 6 to 10 cm H2O, in lung-lavaged rabbits.
吸入一氧化氮可通过改善呼吸窘迫综合征新生儿及急性呼吸窘迫综合征成人的通气/灌注比来提高氧合。有证据表明，当肺仍处于肺不张和充气不良状态时，吸入一氧化氮无效。本研究旨在通过外源性表面活性剂改善肺通气或增加呼气末正压来增强一氧化氮的输送。
实验性对比研究。
一所大型大学的研究实验室。
28只成年新西兰白兔，体重2.7±0.3千克。
通过用盐水反复进行全肺灌洗诱导肺损伤。动物采用潮气量10毫升/千克、吸入氧分数1.0、呼气末正压6厘米水柱进行机械通气。最后一次灌洗后45分钟，将动物随机分为五组。在两组中，在开始吸入一氧化氮之前，首先通过滴注低剂量外源性表面活性剂（25毫克/千克）或增加呼气末正压至10厘米水柱来增加肺通气。在这些动物中的每只动物中，吸入五种不同浓度的一氧化氮（4至20 ppm）30分钟，随后是30分钟的洗脱期。其他三组作为对照组，仅接受一种治疗方案：一氧化氮（4至20 ppm）、表面活性剂（25毫克/千克）或呼气末正压（10厘米水柱）。
灌洗前后，每30分钟测量一次血气和肺力学指标。两种增加肺通气的策略均在30分钟内将动脉血氧分压值从61±13托（8.1±1.7千帕）提高到200至300托（26.6至39.9千帕）。吸入一氧化氮后，仅在接受低剂量（25毫克/千克）表面活性剂的动物中观察到氧合进一步增加。吸入一氧化氮的对照组氧合无显著变化，六只动物中有四只在观察期内死亡。在呼气末正压增加至10厘米水柱的两组中，一半动物在观察期内发生气胸。
这些数据表明，在肺灌洗的兔中，吸入一氧化氮能够通过低剂量外源性表面活性剂实现肺泡复张后改善动脉氧合，而不是通过将呼气末正压从6厘米水柱增加到10厘米水柱来实现。
