title: Acute lung inflammatory response and injury after hemorrhagic shock are more severe in postpartum rabbits.
abstract: OBJECTIVE
  The acute respiratory distress syndrome may complicate postpartum hemorrhagic shock and resuscitation, but its mechanisms are not yet well defined. We studied the lung inflammatory response to postpartum hemorrhagic shock and resuscitation in a rabbit model and the role of the nuclear factor-κB pathway.
  
  
  METHODS
  Randomized, controlled, prospective study.
  
  
  METHODS
  University hospital laboratory.
  
  
  METHODS
  Nonobstetric (not pregnant nor postpartum) and obstetrical (within 2 hrs postpartum) rabbits.
  
  
  METHODS
  Nonobstetric and obstetric female New Zealand white rabbits underwent fixed-pressure or fixed-volume hemorrhagic shock for 30 mins and then were rapidly resuscitated with the shed blood and Ringer's solution. Finally, they were either monitored for survival time or euthanized by exsanguination for lung tissue examination 24 hrs after hemorrhage.
  
  
  RESULTS
  After hemorrhagic shock and resuscitation, median survival time in obstetric rabbits (3 days) was significantly shorter (p<.05) than that in nonobstetric rabbits (5 days). Compared with nonobstetric rabbits, obstetric rabbits had more severe lung injury as indicated by alveolar and interstitial fluid accumulation and marked neutrophil sequestration and greater lung injury score, myeloperoxidase activity, expression of intercellular adhesion molecule-1, serum tumor necrosis factor-α levels, and nuclear factor-κB activation, and lower serum interleukin-10 levels (p<.05 for all).
  
  
  CONCLUSIONS
  After hemorrhage and resuscitation, obstetric rabbits had significantly shorter survival time and more severe lung injury than nonobstetric rabbits. The mechanism may be through upregulation of the signal transductions of the nuclear factor-κB pathways.
authors.affiliation: Department of Obstetrics and Gynecology, Nan Fang Hospital, and Guangdong Province Key Laboratory of Shock and Microcirculation Research, Department of Pathophysiology, Southern Medical University, Guangzhou, China.
authors.forename: Chao
authors.initials: C
authors.lastname: Sheng
authors.forename: Yan-Hong
authors.initials: YH
authors.lastname: Yu
authors.forename: Ke-Seng
authors.initials: KS
authors.lastname: Zhao
authors.forename: Li-Ping
authors.initials: LP
authors.lastname: Huang
authors.forename: Robert F
authors.initials: RF
authors.lastname: Lodato
authors.forename: Zhi-Jian
authors.initials: ZJ
authors.lastname: Wang
authors.forename: Chen-Hong
authors.initials: CH
authors.lastname: Wang
authors.forename: Sui-Hai
authors.initials: SH
authors.lastname: Wang
authors.forename: Ding-Sheng
authors.initials: DS
authors.lastname: Zha
mesh_terms: D055371:Acute Lung Injury / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D000818:Animals; D004195:Disease Models, Animal; D005260:Female; D018799:Intercellular Adhesion Molecule-1 / Q000378:metabolism; D016753:Interleukin-10 / Q000097:blood; D008168:Lung / Q000473:pathology; D016328:NF-kappa B / Q000097:blood; D009195:Peroxidase / Q000378:metabolism; D011014:Pneumonia / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology; D049590:Postpartum Period / Q000502:physiology*; D011247:Pregnancy; D011817:Rabbits; D012771:Shock, Hemorrhagic / Q000150:complications* / Q000503:physiopathology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D016328:NF-kappa B; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D016753:Interleukin-10; D009195:Peroxidase