title: Hypoxic-ischemic brain damage induces distant inflammatory lung injury in newborn piglets.
abstract: BACKGROUND
  We aimed to investigate whether neonatal hypoxic-ischemic (HI) brain injury induces inflammatory lung damage.
  
  
  METHODS
  Thus, hypoxic (HYP, FiO2 10% for 30 min), ischemic (ISC, bilateral carotid flow interruption for 30 min), or HI event was performed in 1-2-d-old piglets. Dynamic compliance (Cdyn), oxygenation index (OI), and extravascular lung water (EVLW) were monitored for 6 h. Then, histologic damage was assessed in brain and lung (lung injury severity score). Total protein content (TPC) was determined in broncoalveolar lavage fluid (BALF), and IL-1β concentration was measured in lung and brain tissues and blood.
  
  
  RESULTS
  Piglets without hypoxia or ischemia served as controls (SHM). HI-induced brain damage was associated with decreased Cdyn, increased OI and EVLW, and histologic lung damage (interstitial leukocyte infiltration, congestive hyperemia, and interstitial edema). BALF TPC was increased, suggesting inflammatory damage. In agreement, tissue IL-1β concentration increased in the brain and lung, in correspondence with increased IL-1β serum concentration. Neither HYP nor ISC alone led to brain or lung damage.
  
  
  CONCLUSIONS
  HI brain damage in newborn piglets led to inflammatory lung damage, suggesting an additional mechanism accounting for the development of lung dysfunction after neonatal HI encephalopathy.
authors.affiliation: Department of Neonatology, Hospital Clínico San Carlos, Madrid, Spain.
authors.forename: Luis
authors.initials: L
authors.lastname: Arruza
authors.affiliation: Health Research Institute Puerta de Hierro Majadahonda, Madrid, Spain.
authors.forename: M Ruth
authors.initials: MR
authors.lastname: Pazos
authors.affiliation: Health Research Institute Puerta de Hierro Majadahonda, Madrid, Spain.
authors.forename: Nagat
authors.initials: N
authors.lastname: Mohammed
authors.affiliation: Department of Pathology, Hospital Clínico San Carlos, Madrid, Spain.
authors.forename: Natalia
authors.initials: N
authors.lastname: Escribano
authors.affiliation: Intensive Care Traslational Research Group, Biocruces Health Research Institute, Bizkaia, Spain.
authors.forename: Hector
authors.initials: H
authors.lastname: Lafuente
authors.affiliation: Health Research Institute Puerta de Hierro Majadahonda, Madrid, Spain.
authors.forename: Martín
authors.initials: M
authors.lastname: Santos
authors.affiliation: Intensive Care Traslational Research Group, Biocruces Health Research Institute, Bizkaia, Spain.
authors.forename: Francisco J
authors.initials: FJ
authors.lastname: Alvarez-Díaz
authors.affiliation: Department of Neonatology, Hospital Clínico San Carlos, Madrid, Spain.|Health Research Institute Puerta de Hierro Majadahonda, Madrid, Spain.
authors.forename: Jose
authors.identifier: http://orcid.org/0000-0003-4405-3545
authors.initials: J
authors.lastname: Martínez-Orgado
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D001921:Brain / Q000378:metabolism / Q000473:pathology*; D001992:Bronchoalveolar Lavage Fluid / Q000737:chemistry; D004195:Disease Models, Animal; D000860:Hypoxia; D020925:Hypoxia-Ischemia, Brain / Q000473:pathology*; D007249:Inflammation; D053583:Interleukin-1beta / Q000378:metabolism; D008168:Lung / Q000378:metabolism* / Q000503:physiopathology; D055370:Lung Injury / Q000473:pathology*; D008297:Male; D013552:Swine
chemical_list: D053583:Interleukin-1beta