| Interaction of endogenous endothelin-1 and inhaled nitric oxide in term and preterm infants. | |
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MedLine Citation:
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PMID: 12193107 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The peptide endothelin-1 (ET-1) plays an unknown role in the pathogenesis and progression of two important neonatal pulmonary disorders, chronic lung disease (CLD) of prematurity and persistent pulmonary hypertension of the newborn (PPHN). Inhaled nitric oxide (INO) is a proven vasodilator therapy in PPHN and is an experimental therapy in CLD. We sought to determine the effects, if any, of the interaction of inhaled INO with ET-1 in these two separate disorders. Infants (n=21) with PPHN (mean gestation age, 39.4 weeks; mean birth weight, 3470 g) were treated with INO. All infants were <72 h of age at baseline. Plasma obtained at baseline and after 24 h of INO therapy was assessed for ET-1. The change in ET-1 levels with INO was inversely correlated with change in arterial partial pressure of O(2) (r=-0.71, P=0.0003). A separate group of 33 patients with CLD (mean gestational age, 27 weeks; mean birth weight, 740 g; mean age, 19 days) had tracheal aspirate levels of ET-1 obtained before, during, and after 7 days' administration of INO. Values were normalized by soluble secretory component of IgA. Tracheal aspirate ET-1 levels were detectable before INO therapy. There was no significant change during or after treatment with INO. There was not a significant correlation between baseline fractional inspired O(2) and ET-1 levels. There was a non-significant trend in the correlation between the change in ET-1 and the change in interleukin-8 levels in tracheal aspirate. This report confirms the presence of ET-1 in tracheal aspirate of premature infants who are developing CLD and reaffirms the presence of ET-1 in plasma of infants with PPHN. Short-term INO therapy was associated with a decrease in plasma ET-1 levels in PPHN, but did not affect tracheal aspirate ET-1 in CLD. Given the vasconstrictive, profibrotic, and proinflammatory properties of ET-1, specific ET-1 receptor antagonists could be considered as candidates for trials as adjunct therapy in either or both of these disorders. |
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Authors:
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William E Truog; Eugenia Pallotto; Perry Clark; Beverly Banks; Harold A Kaftan; Ikechukwu I Ekekezie; Mike Norberg; Roberta A Ballard |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Clinical science (London, England : 1979) Volume: 103 Suppl 48 ISSN: 0143-5221 ISO Abbreviation: Clin. Sci. Publication Date: 2002 Aug |
Date Detail:
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Created Date: 2002-08-23 Completed Date: 2002-11-20 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7905731 Medline TA: Clin Sci (Lond) Country: England |
Other Details:
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Languages: eng Pagination: 294S-297S Citation Subset: IM |
Affiliation:
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Section of Neonatology, Children's Mercy Hospitals and Clinics and Department of Pediatrics, Kansas City School of Medicine, University of Missouri, Kansas City, MO 64108, U.S.A. wtroung@cmh.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Administration, Inhalation Biological Markers / blood Endothelin-1 / blood, metabolism* Humans Hypertension, Pulmonary / drug therapy* Infant, Newborn Infant, Premature Infant, Premature, Diseases / immunology, metabolism Interleukin-8 / blood Nitric Oxide / administration & dosage, metabolism, therapeutic use* Persistent Fetal Circulation Syndrome / immunology, metabolism* Pulmonary Disease, Chronic Obstructive / drug therapy, immunology, metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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K23 HL04264-01/HL/NHLBI NIH HHS; R01-HL-58175/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Biological Markers; 0/Endothelin-1; 0/Interleukin-8; 10102-43-9/Nitric Oxide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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