| Ibuprofen-induced patent ductus arteriosus closure: physiologic, histologic, and biochemical effects on the premature lung. | |
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MedLine Citation:
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PMID: 18450898 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: The goal was to study the pulmonary, biochemical, and morphologic effects of a persistent patent ductus arteriosus in a preterm baboon model of bronchopulmonary dysplasia. METHODS: Preterm baboons (treated prenatally with glucocorticoids) were delivered at 125 days of gestation (term: 185 days), given surfactant, and ventilated for 14 days. Twenty-four hours after birth, newborns were randomly assigned to receive either ibuprofen (to close the patent ductus arteriosus; n = 8) or no drug (control; n = 13). RESULTS: After treatment was started, the ibuprofen group had significantly lower pulmonary/systemic flow ratio, higher systemic blood pressure, and lower left ventricular end diastolic diameter, compared with the control group. There were no differences in cardiac performance indices between the groups. Ventilation index and dynamic compliance were significantly improved with ibuprofen. The improved pulmonary mechanics in ibuprofen-treated newborns were not attributable to changes in levels of surfactant protein B, C, or D, saturated phosphatidylcholine, or surfactant inhibitory proteins. There were no differences in tracheal concentrations of cytokines commonly associated with the development of bronchopulmonary dysplasia. The groups had similar messenger RNA expression of genes that regulate inflammation and remodeling in the lung. Lungs from ibuprofen-treated newborns were significantly drier (lower wet/dry ratio) and expressed 2.5 times more epithelial sodium channel protein than did control lungs. By 14 days after delivery, control newborns had morphologic features of arrested alveolar development (decreased alveolar surface area and complexity), compared with age-matched fetuses. In contrast, there was no evidence of alveolar arrest in the ibuprofen-treated newborns. CONCLUSIONS: Ibuprofen-induced patent ductus arteriosus closure improved pulmonary mechanics, decreased total lung water, increased epithelial sodium channel expression, and decreased the detrimental effects of preterm birth on alveolarization. |
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Authors:
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Donald McCurnin; Steven Seidner; Ling-Yi Chang; Nahid Waleh; Machiko Ikegami; Jean Petershack; Brad Yoder; Luis Giavedoni; Kurt H Albertine; Mar Janna Dahl; Zheng-ming Wang; Ronald I Clyman |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Pediatrics Volume: 121 ISSN: 1098-4275 ISO Abbreviation: Pediatrics Publication Date: 2008 May |
Date Detail:
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Created Date: 2008-05-02 Completed Date: 2008-06-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0376422 Medline TA: Pediatrics Country: United States |
Other Details:
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Languages: eng Pagination: 945-56 Citation Subset: AIM; IM |
Affiliation:
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Department of Pediatrics, University of Texas Health Science Center, San Antonio, Texas, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Animals, Newborn Anti-Inflammatory Agents, Non-Steroidal / therapeutic use* Bronchoalveolar Lavage Fluid / chemistry Ductus Arteriosus, Patent / drug therapy*, metabolism, physiopathology Epithelial Sodium Channel / metabolism Extravascular Lung Water / metabolism Female Fetal Organ Maturity / drug effects Hemodynamics Ibuprofen / therapeutic use* Inflammation Mediators / metabolism Lung / anatomy & histology, drug effects*, embryology, physiology Male Papio papio Phosphatidylcholines / metabolism Pulmonary Surfactant-Associated Proteins / metabolism Respiration |
| Grant Support | |
ID/Acronym/Agency:
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HL46691/HL/NHLBI NIH HHS; HL52636/HL/NHLBI NIH HHS; HL56061/HL/NHLBI NIH HHS; HL56401/HL/NHLBI NIH HHS; HL62875/HL/NHLBI NIH HHS; HL63329/HL/NHLBI NIH HHS; HL63397/HL/NHLBI NIH HHS; HL63399/HL/NHLBI NIH HHS; P51RR13986/RR/NCRR NIH HHS; R24 RR023345/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Anti-Inflammatory Agents, Non-Steroidal; 0/Epithelial Sodium Channel; 0/Inflammation Mediators; 0/Phosphatidylcholines; 0/Pulmonary Surfactant-Associated Proteins; 15687-27-1/Ibuprofen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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