Abstract
ObjectiveAsphyxia of newborns is a severe and frequent challenge of the peri- and postnatal period. The purpose of this study was to study early morphological, immunological and structural alterations in lung tissue after asphyxia and hemorrhage (AH).Methods44 neonatal piglets (age 32 hrs) underwent asphyxia and hemorrhage (AH) and were treated according to the international liaison committee of resuscitation (ILCOR) guidelines. For this study, 15 piglets (blood transfusion (RBC) n = 9; NaCl n = 6, mean age 31 hrs) were randomly picked. 4 hours after ROSC (return of spontaneous circulation), lung tissue and blood samples were collected.ResultsAn elevation of myeloperoxidase (MPO) activity was observed 4 hrs after AH accompanied by an increase of surfactant D after RBC treatment. After AH tight junction proteins Claudin 18 and junctional adhesion molecule 1 (JAM1) were down-regulated, whereas Occludin was increased. Furthermore, after AH and RBC treatment dephosphorylated active form of Connexin 43 was increased.ConclusionsAH in neonatal pigs is associated with early lung injury, inflammation and alterations of tight junctions (Claudin, Occludin, JAM-1) and gap junctions (Connexin 43) in lung tissue, which contributes to the development of lung edema and impaired function.
Highlights
Asphyxia is a common phenomenon during birth and the postnatal period [1], which leads to the annual death of approximately 1 million newborns worldwide [2]
AH in neonatal pigs is associated with early lung injury, inflammation and alterations of tight junctions (Claudin, Occludin, JAM-1) and gap junctions (Connexin 43) in lung tissue, which contributes to the development of lung edema and impaired function
Surfactant D in lung tissue was increased only in the animals treated with red blood cells (RBCs) (Fig 1D), which is shown in representative images of Surfactant D staining (Fig 1E)
Summary
Asphyxia is a common phenomenon during birth and the postnatal period [1], which leads to the annual death of approximately 1 million newborns worldwide [2]. Lung injury occurs in 25% of all asphyxiated newborns, which ranges from a mild respiratory distress to pulmonary hemorrhage/severe respiratory failure [5]. Alveolar edema is an early factor in the development of acute respiratory distress syndrome (ARDS), which results from an increase of the permeability of the alveolar epithelial barrier. Pulmonary edema is associated with increased mortality, as described in the context of acute lung injury (ALI) in adults [7]. ARDS in newborns requires respiratory therapy which is associated with complications such as pneumothorax, pulmonary interstitial emphysema and pneumopericardium [8]. In adults with ARDS alveolar macrophages are activated and release cytokines such as tumor necrosis factor (TNF) and interleukin 1 (IL-1). Pulmonary influx of neutrophils has been correlated to lung injury and increased permeability of the alveolarcapillary membrane [11]
Sign-in/Register to view highlights & summary 
Published Version (
Free)
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
