Lowson S M, Rich G F, McArdle P A, Jaidev J, Morris G N
Department of Anesthesiology, University of Virginia Health Sciences Center, Charlottesville, VA 22098, USA.
Anesth Analg. 1996 Mar;82(3):574-81. doi: 10.1097/00000539-199603000-00026.
We investigated the response to varying concentrations of inhaled nitric oxide (NO) in 18 patients with acute respiratory distress syndrome (ARDS). The study was divided into two parts. In Part 1, 5-40 ppm of inhaled NO was evaluated in 10 patients with ARDS. In Part 2, 0.1-10 ppm of inhaled NO was evaluated in eight patients with ARDS. Inhaled NO significantly (P < 0.05) decreased the mean pulmonary artery pressure (MPAP) and pulmonary vascular resistance index (PVRI), and increased the arterial oxygenation (PaO2) at concentrations of 0.1 to 40 ppm. No dose response was detectable for the pulmonary artery pressure (PAP) or PVRI over this dose range. The increase in PaO2 at 10 ppm of NO was significantly greater than that at 0.1 ppm but not 1 ppm. The decrease in PVRI and the increase in PaO2 were both significantly correlated with the baseline PVRI. While the maximum hemodynamic and oxygenation responses to inhaled NO are achieved at approximately 1 ppm, it appears that the maximum hemodynamic response is observed at lower concentrations (0.1 ppm) of inhaled NO than the improvement in oxygenation (1-10 ppm). Higher concentrations of NO do not produce any further change in these variables. It appears that the baseline PVRI may be the best marker predicting a beneficial response to NO.
我们研究了18例急性呼吸窘迫综合征（ARDS）患者对不同浓度吸入一氧化氮（NO）的反应。该研究分为两部分。在第一部分中，对10例ARDS患者评估了5 - 40 ppm的吸入NO。在第二部分中，对8例ARDS患者评估了0.1 - 10 ppm的吸入NO。在0.1至40 ppm的浓度下，吸入NO显著（P < 0.05）降低了平均肺动脉压（MPAP）和肺血管阻力指数（PVRI），并提高了动脉氧合（PaO2）。在此剂量范围内，未检测到肺动脉压（PAP）或PVRI的剂量反应。10 ppm NO时PaO2的升高显著大于0.1 ppm时，但不大于1 ppm时。PVRI的降低和PaO2的升高均与基线PVRI显著相关。虽然吸入NO的最大血流动力学和氧合反应在约1 ppm时达到，但似乎吸入NO的最大血流动力学反应在较低浓度（0.1 ppm）时观察到，而氧合改善（1 - 10 ppm）则在较高浓度时观察到。更高浓度的NO不会使这些变量产生任何进一步变化。基线PVRI似乎可能是预测对NO有益反应的最佳指标。
