Effect of nitric oxide on in vitro responsiveness of bovine bronchus and pulmonary vessels

Experiments were conducted in bovine isolated bronchi and pulmonary vessels to test whether nitric oxide (NO) could reduce carbachol and hypoxia or KCl (120 mM) induced contraction. Segments of bronchus or pulmonary vessels were slipped around a water-filled balloon connected to a pressure transduce...

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Veröffentlicht in:The European respiratory journal 1995-05, Vol.8 (5), p.755-761
Hauptverfasser: Zhao, W, Guenard, H
Format: Artikel
Sprache:eng
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Zusammenfassung:Experiments were conducted in bovine isolated bronchi and pulmonary vessels to test whether nitric oxide (NO) could reduce carbachol and hypoxia or KCl (120 mM) induced contraction. Segments of bronchus or pulmonary vessels were slipped around a water-filled balloon connected to a pressure transducer, and mounted in 3 ml thermostated chamber filled with Krebs-Henseleit solution equilibrated with different gas mixtures. NO-CO2-N2 mixtures containing 10, 50 or 100 ppm NO were prepared. The effect of methylene blue on intrinsic tone and the bias effect of residual red blood cells were assessed. The results demonstrate that NO has no obvious effect on the intrinsic tone, the force generated by carbachol stimulation, or the spontaneous relaxation after removal of carbachol, in bronchi, with the exception of 100 ppm which increased the relaxing rate in small bronchi. By contrast, 50 and 100 ppm NO caused 53 and 61% decrease in the hypoxia-induced pulmonary arterial contraction, respectively. One hundred ppm NO caused 40, 38, 50 and 66% decrease in the KCl-induced contraction in pulmonary artery (PA), small pulmonary artery (SPA), small pulmonary vein (SPV) and pulmonary vein (PV), respectively. Sodium nitroprusside (10(-5) M) and isoproterenol (10(-5) M) reduced the carbachol-induced increase in bronchial pressure by 80% and nearly 100%, respectively. The residual concentration of haemoglobin in the chamber cannot explain the lack of effect of NO on the bronchi.
ISSN:0903-1936
1399-3003
DOI:10.1183/09031936.95.08050755