Rossaint R, Pison U, Gerlach H, Falke K J
Freie Universität Berlin, Universitätsklinikum Rudolf Virchow, Klinik für Anaesthesiologie und operative Intensivmedizin, Germany.
Eur Heart J. 1993 Nov;14 Suppl I:133-40.
Nitric oxide (NO), an endothelium-derived relaxing factor synthesized from L-arginine by the enzyme NO synthase, has been identified as an important, short-acting, endogenous vasodilator. In patients with pulmonary hypertension, inhaling a low dose of NO as a gaseous vasodilator has been shown to induce selective vasodilation in ventilated lung areas. It achieves this without the disadvantages attributed to systemically infused vasodilators e.g. systemic vasodilation and an increase in pulmonary right-to-left shunt with a consecutive fall in PaO2. Thus, inhaled NO reduces pulmonary hypertension in the severe adult respiratory distress syndrome and in persistent pulmonary hypertension of the newborn, and improves arterial oxygenation by redistributing pulmonary blood flow away from the shunt and towards areas with almost normal ventilation/perfusion ratios. The bronchodilatory effect of NO may be an alternative therapy for treating asthma and bronchospasm.
一氧化氮（NO）是一种由一氧化氮合酶从L-精氨酸合成的内皮源性舒张因子，已被确定为一种重要的短效内源性血管舒张剂。在肺动脉高压患者中，吸入低剂量的NO作为气体血管舒张剂已被证明可在通气的肺区域诱导选择性血管舒张。它实现这一点而没有全身输注血管舒张剂所带来的缺点，例如全身血管舒张和肺右向左分流增加以及随之而来的动脉血氧分压（PaO2）下降。因此，吸入NO可降低严重成人呼吸窘迫综合征和新生儿持续性肺动脉高压患者的肺动脉高压，并通过将肺血流从分流处重新分配到通气/灌注比几乎正常的区域来改善动脉氧合。NO的支气管舒张作用可能是治疗哮喘和支气管痉挛的一种替代疗法。
