Hypoxic-ischemic brain damage induces distant inflammatory lung injury in newborn piglets

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-1 beta 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-1 beta concentration increased in the brain and lung, in correspondence with increased IL-1 beta serum concentration. Neither HYP nor ISC alone led to brain or lung damage. CONCLUSION: 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.