Changes in nasal nitric oxide concentration associated with symptoms of common cold and treatment with a topical nasal decongestant

Changes in nasal nitric oxide concentration associated with symptoms of common cold and treatment with a topical nasal decongestant
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DOI:
10.3109/00016489709113447
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发表时间:
1997-07-01
影响因子:
1.4
通讯作者:
Eccles, R
Eccles, R
中科院分区:
医学4区
文献类型:
--
作者:
Ferguson, EA;Eccles, R

文献摘要

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一氧化氮(NO)是已知的非特异性宿主防御机制中发挥作用。此外,已经提出,NO在呼吸道防御引起普通感冒的病毒中可能是重要的。事实上,先前已经观察到在上呼吸道感染(URTI)期间经口呼出的空气中NO水平升高,我们想进一步研究NO在URTI的宿主反应中的作用。在97名受试者中,在有症状的URTI期间获得总鼻气道阻力(tNAR)和鼻NO水平。其中,80人接受羟甲唑啉或安慰剂喷雾治疗。治疗后60分钟,获得治疗后tNAR和NO水平。4-6周后,当受试者健康时,也重复测量NO(n = 82)。使用化学发光气体分析仪测量NO水平,同时使用后验测压法测量tNAR。平均治疗前NO水平(1063 +/- 541 ppb)显示在用羟甲唑啉治疗后显著降低(827 +/- 373 ppb),p < 0.0001。平均治疗前rNAR为0.42 Pa cm-3 sec-1,在用羟甲唑啉治疗后也显著降低至0.21 Pa Cm-1 sec-1(I < 0.001)。在用羟甲唑啉治疗后,NO水平的变化与tNAR的变化之间没有显著相关性(p,校正为ties = 0.011,p = 0.98)。在URTI期间获得的NO水平(1130 +/- 444 ppb)与健康时获得的值(1197 +/- 361 ppb)相比无显著差异,p = 0.25。这些结果表明,用局部鼻减充血剂喷雾剂治疗导致鼻NO水平降低。我们认为这是羟甲唑啉收缩血管作用的间接结果。由于在URTI期间没有观察到NO水平的变化,我们认为鼻子中负责NO产生的NO合酶与肺部的反应方式不同。
Nitric oxide (NO) is known to play a role in the non-specific host defence mechanism. Furthermore, it has been proposed that NO may be important in respiratory defence against the viruses which cause the common cold. Indeed, elevated NO levels have previously been observed in orally expired air during upper respiratory tract infection (URTI), We wanted to investigate further the role of NO in the host response to URTI. Total nasal airway resistance (tNAR) and nasal NO levels were obtained during symptomatic URTI in 97 subjects. Of these, 80 received treatment with either oxymetazoline or a placebo spray. Post-treatment tNAR and NO levels were obtained 60 min after treatment. Measurements of NO were also repeated 4-6 weeks later, when subjects were healthy, (n = 82). NO levels were measured using a chemiluminescence gas analyser whilst tNAR was measured using posterior rhinomanometry. The mean pre-treatment NO level (1063 +/- 541 ppb) was shown to be reduced significantly after treatment with oxymetazoline (827 +/- 373 ppb), p < 0.0001. The mean pre-treatment rNAR, 0.42 Pa cm(-3) sec(-1), was also reduced significantly to 0.21 Pa Cm-1 sec(-1) (I) < 0.001) after treatment with oxymetazoline. There was no significant correlation between the change in NO levels and change in tNAR following treatment with oxymetazoline (p, corrected for ties = 0.011, p = 0.98). No significant difference was found between NO levels obtained during URTI (1130 +/- 444 ppb) when compared to values obtained when healthy (1197 +/- 361 ppb), p = 0.25. These results demonstrate that treatment with a topical nasal decongestant spray causes a reduction in nasal NO levels. We propose that this occurs as an indirect consequence of the vasoconstrictor actions of oxymetazoline. Since no change in NO levels was observed during URTI, we propose that the NO synthase responsible for NO production in the nose responds in a different manner to that in the lungs.