Published ahead of print on June 7, 2004, doi:10.1164/rccm.200310-1483OC
Am. J. Respir. Crit. Care Med., Volume 170, Number 9, November 2004, 1006-1013
A more recent version of this article appeared on November 1, 2004
Submitted on November 1, 2003
Accepted on June 4, 2004
Pulmonary Vascular Effects of Inhaled Nitric Oxide and Oxygen Tension in Bronchopulmonary Dysplasia
Peter M Mourani1*, D. Dunbar Ivy2, Dexiang Gao3, and Steven H Abman3
1 Department of Pediatrics, Division of Critical Care, The Children's Hospital and University of Colorado Health Sciences Center, Denver, CO, USA,
2 Department of Pediatrics, Division of Cardiology, The Children's Hospital and University of Colorado Health Sciences Center, Denver, CO, USA,
3 Department of Pediatrics, Division of Pulmonary Medicine, The Children's Hospital and University of Colorado Health Sciences Center, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: peter.mourani{at}uchsc.edu.
Pulmonary hypertension contributes significantly to morbidity and mortality in bronchopulmonary dysplasia (BPD), but little is known about the relative contribution of arterial tone, structural remodeling, and vessel density to pulmonary hypertension, especially in older patients. To determine the role of high pulmonary vascular tone in pulmonary hypertension, we studied the acute effects of oxygen tension, inhaled nitric oxide (iNO), and calcium channel blockers (CCB) in 10 patients with BPD who underwent cardiac catheterization for evaluation of pulmonary hypertension. During normoxic conditions, mean pulmonary arterial pressure (PAP) and pulmonary to systemic vascular resistance ratio (PVR/SVR) were 34±3 mm Hg and 0.42±0.07, respectively. In response to hypoxia, PAP and PVR/SVR increased by 50±8% and 82±14%, respectively (p < 0.01). Hyperoxia decreased PVR/SVR by 28±9% (p = 0.05). The addition of iNO treatment (20-40 ppm) to hyperoxia decreased PAP and PVR/SVR by 29±5% (p < 0.01) and 45±6% (p < 0.05) from baseline values, respectively, achieving near normal values. CCB did not alter PAP or PVR/SVR from baseline values. We conclude that hyperoxia plus iNO causes marked pulmonary vasodilatation in older patients with BPD, suggesting that heightened pulmonary vascular tone contributes to pulmonary vascular disease in BPD.
Key words: bronchopulmonary dysplasia, pulmonary hypertension, cardiac catheterization, pulmonary vascular reactivity, nitric oxide
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