Response to inhaled nitric oxide in acute lung injury depends on distribution of pulmonary blood flow prior to its administration.
Response to inhaled nitric oxide in acute lung injury depends on distribution of pulmonary blood flow prior to its administration.
复制标题
DOI：
10.1164/ajrccm.159.2.9806133
复制
发表时间：
1999-02
影响因子：
24.7
通讯作者：
R. Gust;T. McCarthy;J. Kozlowski;A. Stephenson;D. Schuster
中科院分区：
文献类型：
--
作者：
R. Gust;T. McCarthy;J. Kozlowski;A. Stephenson;D. Schuster
急性肺损伤（ALI）对吸入一氧化氮（iNO）的反应，如氧合改善所证明的，是可变的。我们推测iNO的作用可能与iNO前肺血流（PBF）的分布有关。在本研究中，我们评估了iNO对正常健康犬和油酸（OA）诱导的犬ALI模型的PBF的影响。OA组（n = 5）经中心静脉注射OA 0.08ml/kg建立急性肺损伤模型。E+OA组（n = 5）在给予相同剂量OA前30 min给予低剂量内毒素（15 μ g/kg大肠杆菌内毒素）阻断ALI后缺氧性肺血管收缩。使用正电子发射断层扫描（PET）和H215 O测量局部PBF和肺水浓度（LWC）之前和之后进行OA或安慰剂，然后再次在浓度为10，40和0 ppm的iNO。OA损伤后120分钟，仅OA组的PaO 2/FIO 2显著下降，从567 +/- 32降至437 +/- 67 mm Hg。在这些动物中，PBF从肺的背侧水肿区重新分布到非依赖区，从而部分保持正常的通气/灌注关系。在正常动物中，仅在OA组中，iNO没有显著改变PBF或氧合。在E+OA组中，给予低剂量内毒素消除了背侧水肿肺区域的灌注再分布。结果，PaO 2/FIO 2从558 +/- 70降至119 +/- 53 mmHg，降幅明显大于仅OA组。在E+OA组中，iNO给药使灌注再分布恢复到与仅OA组相似的水平，这与PaO 2/FIO 2显著改善相关，从119 +/- 53改善至251 +/- 159（10 ppm iNO）和259 +/- 165 mmHg（40 ppm iNO）。我们的结论是，急性肺损伤后iNO对氧合的影响取决于前iNO灌注模式，这可能有助于解释在急性呼吸窘迫综合征患者中经常观察到的对iNO的可变反应。
Responses to inhaled nitric oxide (iNO) in acute lung injury (ALI), as evidenced by improvements in oxygenation, are variable. We hypothesized that the effect of iNO may be related to the pre-iNO distribution of pulmonary blood flow (PBF). In the present study we evaluated the effect of iNO on PBF in normal healthy dogs and in a canine model of ALI induced by oleic acid (OA). In Group "OA only" (n = 5), ALI was induced by central venous injection of 0.08 ml/kg OA. In Group "E+OA" (n = 5), hypoxic pulmonary vasoconstriction after ALI was blocked with low-dose endotoxin (15 microg/kg of Escherichia coli endotoxin) administered 30 min before giving the same dose of OA. Measurements of regional PBF and lung water concentration (LWC) using positron emission tomography (PET) and H215O were performed before and after OA or placebo, and then again at concentrations of 10, 40, and 0 ppm iNO. One hundred twenty minutes after OA injury, PaO2/FIO2 fell significantly in Group OA only, from 567 +/- 32 to 437 +/- 67 mm Hg. In these animals, PBF redistributed from the dorsal edematous regions of the lungs to the nondependent zones, thus partially preserving normal ventilation/ perfusion relationships. As in the normal animals, in Group OA only, iNO did not significantly change either PBF or oxygenation. In Group E+OA, the administration of low-dose endotoxin eliminated perfusion redistribution from the dorsal edematous lung regions. As a result, PaO2/FIO2 fell from 558 +/- 70 to 119 +/- 53 mm Hg, a decrease that was significantly greater than that in Group OA only. In Group E+OA, administration of iNO restored perfusion redistribution to a similar level as in Group OA only, which was associated with a significant improvement in PaO2/FIO2, from 119 +/- 53 to 251 +/- 159 (10 ppm iNO), and 259 +/- 165 mm Hg (40 ppm iNO). We conclude that the effect of iNO on oxygenation after ALI depends on the pre-iNO perfusion pattern, which may help explain the variable response to iNO often observed in patients with acute respiratory distress syndrome.