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Laboratory and Animal Investigations |

Prolonged Nitric Oxide Inhalation Fails to Regress Hypoxic Vascular Remodeling in Rat Lung*

Bao Hua Jiang, MD; Junko Maruyama, MD; Ayumu Yokochi, MD; Manabu Iwasaki, MD; Homare Amano, MD; Yoshihide Mitani, MD; Kazuo Maruyama, MD
Author and Funding Information

*From the Department of Anesthesiology and the Intensive Care Unit (Drs. Jiang, Yokochi, Iwasaki, Amano, and K. Maruyama), and Departments of Physiology (Dr. J. Maruyama) and Pediatrics (Dr. Mitani), Faculty of Medicine, University of Mie, Japan.

Correspondence to: Kazuo Maruyama, MD, Department of Anesthesiology, Mie University School of Medicine, 2-174, Edobashi, Tsu, Mie, Japan 514-8507; e-mail: masuika@clin.medic.mie-u.ac.jp



Chest. 2004;125(6):2247-2252. doi:10.1378/chest.125.6.2247
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Study objective: The purpose of present study was to investigate whether long-term nitric oxide (NO) inhalation during the recovery in air might improve the regression of chronic hypoxic pulmonary hypertension (PH) and vascular changes.

Materials and methods: The rats were exposed to 10 ppm of NO in air for 10 days (n = 12) and 30 days (n = 4), or 40 ppm of NO in air for 10 days (n = 6) and 30 days (n = 12) following 10 days of hypobaric hypoxia (380 mm Hg, 10% oxygen). For each NO group, air control rats following hypoxic exposure were studied at the same time (n = 13, 11, 9, and 11, respectively). Normal air rats (n = 6) without hypoxic exposure and rats (n = 7) following 10 days of hypoxic exposure were used as normal and chronic hypoxic control groups, respectively. Muscularization of normally nonmuscular peripheral arteries and medial hypertrophy of normally muscular arteries were assessed by light microscopy. An additional 16 rats were used to investigate the recovery of pulmonary artery pressure with (n = 8) and without NO inhalation (n = 8) after 10 days of hypobaric hypoxia.

Results: Long-term hypoxia-induced PH, right ventricular hypertrophy (RVH), and hypertensive pulmonary vascular changes, each of which regressed partly after recovery in room air. There were no differences among rats with and without NO during each recovery period in RVH, medial wall thickness of muscular artery, and the percentages of muscularized arteries at the alveolar wall and duct levels. Continuous inhaled 40 ppm NO decreased pulmonary artery pressure from 40.1 ± 1.1 to 29.9 ± 3.8 mm Hg (mean ± SE) [n = 8], which was not different in the rats without NO inhalation (n = 8). Urine nitrate level was higher in rats that had inhaled NO.

Conclusion: Continuous NO inhalation showed no effect on regression of pulmonary vascular remodeling in chronic hypoxic PH after returning to room air.

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