Heller H, Hoffmann G, Schobersberger W, Schuster K D
Department of Physiology, University of Bonn, Germany.
Acta Physiol Scand. 1997 Nov;161(3):311-5. doi: 10.1046/j.1365-201X.1997.00232.x.
In five mechanically ventilated rabbits, we studied the property of inhaled nitric oxide in helping to treat hypoxaemia which was induced by intravenous endotoxin (Escherichia coli-derived lipopolysaccharide, serotype 0111: B4). We used measurements of arterial partial pressure of oxygen to check a therapeutic nitric oxide benefit. Pulmonary artery pressure was continuously monitored. Furthermore, we determined the single-breath diffusing capacity for nitric oxide. Measurements of plasma nitrite/nitrate concentration served as an indicator of endogenous nitric oxide output. The first infusion of endotoxin led to a transient pulmonary vasoconstriction, whereas arterial partial pressure of oxygen was permanently reduced by 30 +/- 10 mmHg (mean +/- SD), attaining minimal values of 48 +/- 3.4 mmHg due to additional endotoxin. Single-breath diffusing capacity for nitric oxide declined by 20 +/- 5.5% of baseline values until the experiments were concluded. Endotoxin induced an increase in plasma nitrite/nitrate concentration in the five rabbits as well as in the control animals (four rabbits) without exogenous nitric oxide supply. During the 25 inhalations of nitric oxide (3-50 ppm), arterial oxygenation did not change significantly. Thus endotoxin permanently impaired pulmonary gas exchange without inducing pulmonary hypertension. Inhaled nitric oxide did not improve arterial oxygenation during endotoxaemia.
在五只机械通气的兔子身上，我们研究了吸入一氧化氮对治疗由静脉注射内毒素（大肠杆菌来源的脂多糖，血清型0111：B4）诱导的低氧血症的作用。我们通过测量动脉血氧分压来检验一氧化氮的治疗效果。持续监测肺动脉压力。此外，我们测定了一氧化氮的单次呼吸弥散能力。血浆亚硝酸盐/硝酸盐浓度的测量作为内源性一氧化氮输出的指标。首次注射内毒素导致短暂的肺血管收缩，而动脉血氧分压因额外注射内毒素而永久性降低30±10 mmHg（平均值±标准差），最低值达到48±3.4 mmHg。直到实验结束，一氧化氮的单次呼吸弥散能力下降至基线值的20±5.5%。内毒素使五只兔子以及未供应外源性一氧化氮的对照动物（四只兔子）的血浆亚硝酸盐/硝酸盐浓度升高。在25次吸入一氧化氮（3 - 50 ppm）期间，动脉氧合没有显著变化。因此，内毒素永久性损害肺气体交换但未诱发肺动脉高压。在内毒素血症期间，吸入一氧化氮并不能改善动脉氧合。
