Stuart-Smith K, Bynoe T C, Lindeman K S, Hirshman C A
Department of Anesthesiology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
J Appl Physiol (1985). 1994 Sep;77(3):1142-7. doi: 10.1152/jappl.1994.77.3.1142.
Nitrovasodilators and nitric oxide relax airway smooth muscle. The mechanism by which nitrovasodilators are thought to act is by release of nitric oxide, but the importance of nitric oxide in nitrovasodilator-induced airway smooth muscle relaxation is unclear. The aim of this study was to compare the relaxing effects of nitric oxide itself with those of nitrovasodilators in porcine tracheal muscle and intrapulmonary airways and to investigate the mechanisms involved. Strips of porcine tracheal smooth muscle, rings of bronchi, and strips of bronchi from the same animal were suspended in organ chambers in modified Krebs Ringer solution (95% O2-5% CO2, 37 degrees C). Tissues were contracted with carbachol, and concentration-response curves to nitric oxide, sodium nitroprusside, and SIN-1 (an active metabolite of molsidomine) were obtained. All tissues relaxed to sodium nitroprusside, SIN-1, and nitric oxide. The relaxation to nitric oxide but not to SIN-1 or sodium nitroprusside was inhibited by methylene blue. Tissues pretreated with methylene blue that failed to relax to nitric oxide were, however, relaxed by sodium nitroprusside. These results demonstrate that nitrovasodilators relax airways by a mechanism other than by or in addition to the release of nitric oxide.
硝基血管扩张剂和一氧化氮可使气道平滑肌松弛。人们认为硝基血管扩张剂的作用机制是通过释放一氧化氮，但一氧化氮在硝基血管扩张剂诱导的气道平滑肌松弛中的重要性尚不清楚。本研究的目的是比较一氧化氮本身与硝基血管扩张剂对猪气管肌肉和肺内气道的松弛作用，并研究其中涉及的机制。将来自同一动物的猪气管平滑肌条、支气管环和支气管条悬挂在装有改良克雷布斯林格溶液（95% O₂ - 5% CO₂，37℃）的器官浴槽中。用卡巴胆碱使组织收缩，然后获得对一氧化氮、硝普钠和SIN - 1（吗多明的活性代谢产物）的浓度 - 反应曲线。所有组织对硝普钠、SIN - 1和一氧化氮均有松弛反应。亚甲蓝抑制了对一氧化氮的松弛反应，但未抑制对SIN - 1或硝普钠的松弛反应。然而，用亚甲蓝预处理后对一氧化氮无松弛反应的组织，对硝普钠仍有松弛反应。这些结果表明，硝基血管扩张剂通过释放一氧化氮之外的机制或除释放一氧化氮之外还通过其他机制使气道松弛。
