Inhaled nitric oxide attenuates bronchoconstriction in canine peripheral airways.

Inhaled nitric oxide attenuates bronchoconstriction in canine peripheral airways.
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吸入一氧化氮可减弱犬外周气道中的支气管收缩。

DOI:
10.1164/ajrccm.153.2.8564105
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发表时间:
1996
期刊:
American journal of respiratory and critical care medicine.
影响因子:
--
通讯作者:
Hirshman,CA
Hirshman,CA
中科院分区:
--
文献类型:
--
作者:
Gwyn,DR;Lindeman,KS;Hirshman,CA

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吸入一氧化氮已被提议作为支气管扩张剂,因为它可以放松血管和气道平滑肌并减弱胆碱能反射。尽管吸入一氧化氮已被证明可作为中央气道的支气管扩张剂,但对周围气道的影响很大程度上未知。为了确定一氧化氮是否会直接松弛外周气道,我们研究了一氧化氮减轻麻醉狗外周气道中低碳酸血症和乙酰胆碱引起的收缩的能力。使用楔形支气管镜技术测量外周气道阻力(RP)。在存在或不存在一氧化氮的情况下,通过低碳酸血症(通过支气管镜检查 0% CO2,持续 3 分钟)或雾化乙酰胆碱(30 至 60 微克/毫升,持续 1 至 3 分钟)可增加 RP。在没有氧气的情况下,一氧化氮直接输送到肺周围。一氧化氮 (14.5 至 250 ppm) 可使低碳酸血症反应减弱 38 +/- 0 至 74 +/- 0% (n = 6),使乙酰胆碱反应减弱 36 +/- 0 至 52 +/- 0% (n = 6)。吸入一氧化氮 (< 100 ppm) 能够减弱 Rp 对两种不同直接作用刺激的反应,这表明一氧化氮在肺外周起到支气管扩张剂的作用。这种作用的机制可能涉及气道和/或血管平滑肌的松弛。
Inhaled nitric oxide has been proposed as a bronchodilator because it relaxes vascular and airway smooth muscle and attenuates cholinergic reflexes. Although inhaled nitric oxide has been shown to act as a bronchodilator in central airways, effects on peripheral airways are largely unknown. To determine whether nitric oxide produces direct relaxation of peripheral airways, we investigated the ability of nitric oxide to attenuate hypocapnia- and acetylcholine-induced constriction in the peripheral airways of anesthetized dogs. Peripheral airway resistance (RP) was measured using a wedged bronchoscope technique. RP was increased by either hypocapnia (0% CO2 through the bronchoscope for 3 min) or by aerosolized acetylcholine (30 to 60 micrograms/ml for 1 to 3 min), in the presence or absence of nitric oxide. Nitric oxide was delivered directly to the lung periphery in the absence of O2. Nitric oxide (14.5 to 250 ppm) attenuated responses to hypocapnia by 38 +/- 0 to 74 +/- 0% (n = 6) and to acetylcholine by 36 +/- 0 to 52 +/- 0% (n = 6). The ability of inhaled nitric oxide (< 100 ppm) to attenuate Rp responses to two different direct-acting stimuli suggests that nitric oxide acts as a bronchodilator in the lung periphery. The mechanism for this effect may involve relaxation of airway and/or vascular smooth muscle.