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Bilirubin influence on oxidative lung damage and surfactant surface tension properties
Author(s) -
Dani Carlo,
Martelli Elena,
Tronchin Michele,
Buonocore Giuseppe,
Longini Mariangela,
Di Filippo Alessandro,
Giossi Massimo,
Rubaltelli Firmino F.
Publication year - 2004
Publication title -
pediatric pulmonology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.866
H-Index - 106
eISSN - 1099-0496
pISSN - 8755-6863
DOI - 10.1002/ppul.20045
Subject(s) - pulmonary surfactant , medicine , bilirubin , lung , saline , respiratory distress , respiratory disease , respiratory system , gastroenterology , anesthesia , pathology , biochemistry , chemistry
To study the hypothesis that hyperbilirubinemia might reduce in vivo oxidative lung damage while also diminishing lung surfactant surface tension properties during acute lung injury, we performed a randomized study in a rabbit model of acute lung injury. Twenty rabbits were randomized to receive bilirubin or saline intravenously. Acute lung injury was induced by lung lavages with saline. Lung tissue oxidation was evaluated by measuring total hydroperoxide (TH), advanced oxidation protein products (AOPP), and protein carbonyls (PC) in bronchial aspirate (BA) samples. Surface surfactant activity was studied in BA samples using a capillary surfactometer. Bilirubin BA concentration increased in bilirubin‐treated rabbits, while it remained undetectable in controls. A similar increase in TH, AOPP, and PC bronchial aspirate concentrations was found in both the study and control groups, while surfactant surface activity was lower in the bilirubin than in the control group. We conclude that during hyperbilirubinemia, bilirubin enters the lung tissue, where it can be detected in BA fluid. Bilirubin is not effective as an antioxidant agent and exerts a detrimental effect on lung surfactant surface tension properties. These findings may have relevance to the management of premature neonates suffering from respiratory distress syndrome and hyperbilirubinemia. Pediatr Pulmonol. © 2004 Wiley‐Liss, Inc.