Prolonged nitric oxide inhalation during recovery from chronic hypoxia does not decrease nitric oxide-dependent relaxation in pulmonary arteries
Prolonged nitric oxide inhalation during recovery from chronic hypoxia does not decrease nitric oxide-dependent relaxation in pulmonary arteries
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DOI:
10.1378/chest.126.6.1919
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发表时间:
2004-12-01
期刊:
影响因子:
9.6
通讯作者:
Miyasaka, K
中科院分区:
文献类型:
--
作者:
Maruyama, J;Jiang, BH;Miyasaka, K
Study objective: To investigate the effects of long-term nitric oxide (NO) inhalation on the recovery process of right ventricular hypertrophy (RVH) and functional alterations in the NO-cyciic guanosine monophosphate (cGMP) relaxation pathway in rat conduit pulmonary arteries (PAs) in established chronic hypoxic pulmonary hypertension.Materials and methods: A total of 35 rats were exposed to chronic hybaric hypoxia (380 mm Hg, 10% oxygen), and 39 rats were exposed to air for 10 days. Both groups were then exposed to 3 or 10 days of NO 10 ppm, NO 40 ppm, or air (control groups for each NO concentration), resulting in a total of 16 groups. Acetylcholine- and sodium nitroprusside (SNP)-induced relaxation were evaluated in precontracted PA rings. RVH was assessed by heart weight ratio of right ventricle to left ventricle plus septum.Results: NO inhalation had no effect on either the regression of RVH or the recovery process of iinpaired relaxation induced by acetylcholine or SNP in a endothelium-intact hypertensive conduit extrapulmonary artery or intrapulmonary artery (IPA). in a normal endothelium-intact conduit IPA, 40 ppm NO inhalation for 10 days partially augmented SNP-induced relaxation. but not that induced by acetylcholine.Conclusion: Continuous NO inhalation did not affect the regression process of either established RVH or the impaired endogenous NO-cGMP relaxation cascade in a conduit PA in rats during the recovery period after chronic hypoxia.