• Chao Sheng, Yan-Hong Yu, Ke-Seng Zhao, Li-Ping Huang, Robert F Lodato, Zhi-Jian Wang, Chen-Hong Wang, Sui-Hai Wang, and Ding-Sheng Zha.
• 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.
• Crit. Care Med. 2012 May 1; 40 (5): 1570-7.

ObjectiveThe 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.DesignRandomized, controlled, prospective study.SettingUniversity hospital laboratory.SubjectsNonobstetric (not pregnant nor postpartum) and obstetrical (within 2 hrs postpartum) rabbits.InterventionsNonobstetric 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.Measurements And Main ResultsAfter 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).ConclusionsAfter 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.

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