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Human surfactant treatment of severe respiratory distress syndrome: pulmonary effluent indicators of lung inflammation

Academic Article
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Overview

authors

  • Merritt, T. A.
  • Hallman, M.
  • Holcomb, K.
  • Strayer, D.
  • Bloom, B.
  • Revak, S.
  • Cochrane, Charles

publication date

  • May 1986

journal

  • Journal of Pediatrics  Journal

abstract

  • Pulmonary effluent from infants who received exogenous human surfactant for severe respiratory distress syndrome was evaluated for inflammatory changes previously identified with lung injury during the first 2 weeks after birth. The number of pulmonary effluent inflammatory cells was higher only on day 1 in infants given surfactant. No other evidence of enhanced inflammation was detected in cytologic assessment of tracheal secretions. The classical pathway of complement was not activated in infants given surfactant or in control infants 2 weeks after birth. Albumin content of airway secretions was higher on the first day but not significantly altered on subsequent days. Human surfactant treatment was not associated with increased proteolytic activity, measured as neutrophilic elastase per milligram of albumin in lung effluent, but was associated with significantly higher alpha 1-proteinase inhibitor levels than in control infants from days 2 to 7 after birth. These findings provide evidence that exogenous human surfactant instilled into the lungs of preterm infants with severe respiratory distress syndrome is not associated with enhanced lung inflammation, compared with conventional mechanical ventilation alone. These data support additional clinical trials using human surfactant.

subject areas

  • Albumins
  • Blood Proteins
  • Complement Pathway, Classical
  • Exudates and Transudates
  • Humans
  • Infant, Low Birth Weight
  • Infant, Newborn
  • Pancreatic Elastase
  • Pulmonary Surfactants
  • Respiratory Distress Syndrome, Newborn
  • alpha 1-Antitrypsin
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Identity

International Standard Serial Number (ISSN)

  • 0022-3476

Digital Object Identifier (DOI)

  • 10.1016/s0022-3476(86)81058-7

PubMed ID

  • 3486264
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Additional Document Info

start page

  • 741

end page

  • 748

volume

  • 108

issue

  • 5

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