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(Chest. 2004;126:1919-1925.)
© 2004 American College of Chest Physicians

Prolonged Nitric Oxide Inhalation During Recovery From Chronic Hypoxia Does Not Decrease Nitric Oxide-Dependent Relaxation in Pulmonary Arteries*

Junko Maruyama, MD; Bao Hua Jiang, MD; Kazuo Maruyama, MD; Masao Takata, MD and Katsuyuki Miyasaka, MD

* From the Departments of Physiology (Dr. J. Maruyama) and Anesthesiology (Drs. Jiang and K. Maruyama), Mie University School of Medicine, Mie; and Pathophysiology Research Laboratory (Drs. Takata and Miyasaka), National Children’s Medical Research Center, Tokyo, Japan.

Correspondence to: Junko Maruyama, MD, Department of Physiology, Mie University School of Medicine, 2-174, Edobashi, Tsu, Mie 514-8507, Japan; e-mail: j-maru{at}doc.medic.mie-u.ac.jp

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-cyclic 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 hypobaric 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 impaired 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.

Key Words: acetylcholine • hypoxia • nitric oxide • pulmonary hypertension • recovery • right ventricular hypertrophy • sodium nitroprusside • vasodilation






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