Document Detail

Inhaled nitric oxide, oxygen, and alkalosis: dose-response interactions in a lamb model of pulmonary hypertension.
MedLine Citation:
PMID:  10406044     Owner:  NLM     Status:  MEDLINE    
Inhaled nitric oxide (NO) is currently used as an adjuvant therapy for a variety of pulmonary hypertensive disorders. In both animal and human studies, inhaled NO induces selective, dose-dependent pulmonary vasodilation. However, its potential interactions with other simultaneously used pulmonary vasodilator therapies have not been studied. Therefore, the objective of this study was to determine the potential dose-response interactions of inhaled NO, oxygen, and alkalosis therapies. Fourteen newborn lambs (age 1-6 days) were instrumented to measure vascular pressures and left pulmonary artery blood flow. After recovery, the lambs were sedated and mechanically ventilated. During steady-state pulmonary hypertension induced by U46619 (a thromboxane A2 mimic), the lambs were exposed to the following conditions: Protocol A, inhaled NO (0, 5, 40, and 80 ppm) and inspired oxygen concentrations (FiO2) of 0.21, 0.50, and 1.00; and Protocol B, inhaled NO (0, 5, 40, and 80 ppm) and arterial pH levels of 7.30, 7.40, 7.50, and 7.60. Each condition (in randomly chosen order) was maintained for 10 min, and all variables were allowed to return to baseline between conditions. Inhaled NO, oxygen, and alkalosis produced dose-dependent decreases in mean pulmonary arterial pressures (P < 0.05). Systemic arterial pressure remained unchanged. At 5 ppm of inhaled NO, alkalosis and oxygen induced further dose-dependent decreases in mean pulmonary arterial pressures (P < 0.05). At inhaled NO doses > 5 ppm, alkalosis induced further dose-independent decreases in mean pulmonary arterial pressure, while oxygen did not. We conclude that in this animal model, oxygen, alkalosis, and inhaled NO induced selective, dose-dependent pulmonary vasodilation. However, when combined, a systemic arterial pH > 7.40 augmented inhaled NO-induced pulmonary vasodilation, while an FiO2 > 0.5 did not. Therefore, weaning high FiO2 during inhaled NO therapy should be considered, since it may not diminish the pulmonary vasodilating effects. Further studies are warranted to guide the clinical weaning strategies of these pulmonary vasodilator therapies.
R S Heidersbach; M J Johengen; J M Bekker; J R Fineman
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Pediatric pulmonology     Volume:  28     ISSN:  8755-6863     ISO Abbreviation:  Pediatr. Pulmonol.     Publication Date:  1999 Jul 
Date Detail:
Created Date:  1999-09-14     Completed Date:  1999-09-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8510590     Medline TA:  Pediatr Pulmonol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  3-11     Citation Subset:  IM    
Department of Pediatrics, University of California at San Francisco 94143-0106, USA.
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MeSH Terms
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid
Administration, Inhalation
Alkalosis / etiology*,  physiopathology
Analysis of Variance
Animals, Newborn
Disease Models, Animal
Dose-Response Relationship, Drug
Drug Interactions
Hydrogen-Ion Concentration / drug effects
Hypertension, Pulmonary / chemically induced,  drug therapy*,  therapy
Linear Models
Nitric Oxide / administration & dosage*
Oxygen / administration & dosage*
Respiratory Function Tests
Treatment Outcome
Vasodilation / drug effects,  physiology
Reg. No./Substance:
10102-43-9/Nitric Oxide; 76898-47-0/15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5,13-dienoic Acid; 7782-44-7/Oxygen

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