Lundberg J O, Settergren G, Gelinder S, Lundberg J M, Alving K, Weitzberg E
Department of Physiology and Pharmacology, Karolinska Institute, Stockholm, Sweden.
Acta Physiol Scand. 1996 Dec;158(4):343-7. doi: 10.1046/j.1365-201X.1996.557321000.x.
The vasodilator gas nitric oxide (NO) is produced in the paranasal sinuses and is excreted continuously into the nasal airways of humans. This NO will normally reach the lungs with inspiration, especially during nasal breathing. We wanted to investigate the possible effects of low-dose inhalation of NO from the nasal airways on pulmonary function. The effects of nasal and oral breathing on transcutaneous oxygen tension (tcPO2) were studied in healthy subjects. Furthermore, we also investigated whether restoring low-dose NO inhalation would influence pulmonary vascular resistance index (PVRI) and arterial oxygenation (PaO2) in intubated patients who are deprived of NO produced in the nasal airways. Thus, air derived from the patient's own nose was aspirated and led into the inhalation limb of the ventilator. In six out of eight healthy subjects tcPO2 was 10% higher during periods of nasal breathing when compared with periods of oral breathing. In six out of six long-term intubated patients PaO2 increased by 18% in response to the addition of nasal air samples. PVRI was reduced by 11% in four of 12 short-term intubated patients when nasal air was added to the inhaled air. The present study demonstrates that tcPO2 increases during nasal breathing compared with oral breathing in healthy subjects. Furthermore, in intubated patients, who are deprived of self-inhalation of endogenous NO. PaO2 increases and pulmonary vascular resistance may decrease by adding NO-containing air, derived from the patient's own nose, to the inspired air. The involvement of self-inhaled NO in the regulation of pulmonary function may represent a novel physiological principle, namely that of an enzymatically produced airborne messenger. Furthermore, our findings may help to explain one biological role of the human paranasal sinuses.
血管舒张气体一氧化氮（NO）在鼻窦中产生，并持续排入人类的鼻腔气道。这种NO通常会在吸气时到达肺部，尤其是在鼻腔呼吸时。我们想要研究从鼻腔气道低剂量吸入NO对肺功能可能产生的影响。我们研究了健康受试者鼻腔呼吸和口腔呼吸对经皮氧分压（tcPO2）的影响。此外，我们还研究了恢复低剂量NO吸入是否会影响那些被剥夺了鼻腔气道产生的NO的插管患者的肺血管阻力指数（PVRI）和动脉氧合（PaO2）。因此，将源自患者自身鼻子的空气抽出并导入呼吸机的吸入支路。在八名健康受试者中，有六名在鼻腔呼吸期间的tcPO2比口腔呼吸期间高10%。在六名长期插管患者中，有六名患者在添加鼻腔空气样本后PaO2增加了18%。在12名短期插管患者中，有四名在吸入空气中添加鼻腔空气后PVRI降低了11%。本研究表明，与口腔呼吸相比，健康受试者在鼻腔呼吸时tcPO2会升高。此外，在被剥夺内源性NO自主吸入的插管患者中，通过向吸入空气中添加源自患者自身鼻子的含NO空气，PaO2会升高，肺血管阻力可能会降低。自主吸入的NO参与肺功能调节可能代表了一种新的生理原理，即一种酶促产生的气态信使的原理。此外，我们的研究结果可能有助于解释人类鼻窦的一种生物学作用。
