Document Detail

Positive end-expiratory pressure and surfactant decrease lung injury during initiation of ventilation in fetal sheep.
MedLine Citation:
PMID:  21856815     Owner:  NLM     Status:  MEDLINE    
The initiation of ventilation in preterm, surfactant-deficient sheep without positive end-expiratory pressure (PEEP) causes airway injury and lung inflammation. We hypothesized that PEEP and surfactant treatment would decrease the lung injury from initiation of ventilation with high tidal volumes. Fetal sheep at 128-day gestational age were randomized to ventilation with: 1) no PEEP, no surfactant; 2) 8-cmH(2)O PEEP, no surfactant; 3) no PEEP + surfactant; 4) 8-cmH(2)O PEEP + surfactant; or 5) control (2-cmH(2)O continuous positive airway pressure) (n = 6-7/group). After maternal anesthesia and hysterotomy, the head and chest were exteriorized, and the fetus was intubated. While maintaining placental circulation, the fetus was ventilated for 15 min with a tidal volume escalating to 15 ml/kg using heated, humidified, 100% nitrogen. The fetus then was returned to the uterus, and tissue was collected after 30 min for evaluation of early markers of lung injury. Lambs receiving both surfactant and PEEP had increased dynamic compliance, increased static lung volumes, and decreased total protein and heat shock proteins 70 and 60 in bronchoalveolar lavage fluid compared with other groups. Ventilation, independent of PEEP or surfactant, increased mRNA expression of acute phase response genes and proinflammatory cytokine mRNA in the lung tissue compared with controls. PEEP decreased mRNA for cytokines (2-fold) compared with groups receiving no PEEP. Surfactant administration further decreased some cytokine mRNAs and changed the distribution of early growth response protein-1 expression. The use of PEEP during initiation of ventilation at birth decreased early mediators of lung injury. Surfactant administration changed the distribution of injury and had a moderate additive protective effect.
Noah H Hillman; Ilias Nitsos; Clare Berry; J Jane Pillow; Suhas G Kallapur; Alan H Jobe
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2011-08-19
Journal Detail:
Title:  American journal of physiology. Lung cellular and molecular physiology     Volume:  301     ISSN:  1522-1504     ISO Abbreviation:  Am. J. Physiol. Lung Cell Mol. Physiol.     Publication Date:  2011 Nov 
Date Detail:
Created Date:  2011-11-02     Completed Date:  2011-12-22     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100901229     Medline TA:  Am J Physiol Lung Cell Mol Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  L712-20     Citation Subset:  IM    
Cincinnati Children's Hospital Medical Center, Division of Pulmonary Biology, 3333 Burnet Ave., Cincinnati, OH 45229-3039, USA.
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MeSH Terms
Blotting, Western
Bronchoalveolar Lavage Fluid / chemistry
Cytokines / analysis,  biosynthesis
Fetus / metabolism*,  pathology,  physiopathology
Gestational Age
Heat-Shock Proteins / analysis,  biosynthesis
In Situ Hybridization
Infant, Newborn
Infant, Premature, Diseases / metabolism*,  pathology,  physiopathology,  prevention & control*
Lung / metabolism*,  pathology,  physiopathology
Lung Injury / metabolism*,  pathology,  physiopathology
Positive-Pressure Respiration*
Pulmonary Surfactants / administration & dosage,  therapeutic use*
RNA, Messenger / analysis,  biosynthesis
Respiratory Distress Syndrome, Newborn / metabolism*,  physiopathology
Sheep, Domestic
Tidal Volume
Grant Support
Reg. No./Substance:
0/Cytokines; 0/Heat-Shock Proteins; 0/Pulmonary Surfactants; 0/RNA, Messenger

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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