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A Mouse Model of Acute Lung Injury in Pregnancy
Abstract Number: F-42
Abstract Type: Original Research
Rationale: Acute lung injury (ALI) is an under appreciated contributor to morbidity among pregnant women. It is estimated that 25% of pregnant women admitted to the ICU are there due to ALI secondary to infection. Acute respiratory distress syndrome (ARDS) has been found to complicate roughly one out of 6,000 deliveries, which is a shocking 10 times higher prevalence than what is seen in the general population. Some have suggested that pregnancy is a risk factor for severe ALI or ARDS, however, a mechanistic understanding of severe ALI and the increased incidence of ARDS during pregnancy is completely lacking. To better understand the nature of ALI in the parturient, we developed a mouse model of ventilator induced lung injury (VILI) in pregnancy.
Methods: 18+ days pregnant (P) or non-pregnant (NP) mice were subjected to either “protective” (LV) (TV 7ml/kg pre-pregnancy weight, RR 150/min, PEEP 3cm H2O) or “injurious” (HV) (TV 30ml/kg pre-pregnancy weight, RR 50/min, PEEP 0cm H2O) ventilation for 6 hours. Non-ventilated (NV) control animals are also included for comparison.
Results: When comparing the peak airway pressures generated before and after injurious ventilation, the peak airway pressures in non-pregnant mice increase by about 10% whereas the peak airway pressures in pregnant mice increase by nearly 25%. Bronchoalveolar levage (BAL) protein content was found to be twice as high in pregnant as compared to non-pregnant mice exposed to injurious ventilation (figure). BAL protein levels in pregnant mice exposed to protective ventilation were found to be elevated well above BAL protein levels seen in non-pregnant mice exposed to protective ventilation. On histology, we were able to identify both inflammatory cell infiltration into the alveolar space and alveolar protein infiltrates in the lungs of pregnant animals exposed to injurious ventilation, but not in non-pregnant animals exposed to high volume ventilation. Using staining against CD45, we have been able to positively identify increased numbers of immune cells in the injured pregnant lungs as compared to the injured non-pregnant lungs.
Conclusions: In response to injurious ventilation, lungs of pregnant mice, as compared to lungs of non-pregnant mice, display worsened injury as assessed by a number of indices. With further studies into the molecular mechanism of injury, this model of ALI in the parturient may hold a key to understanding the effects of pregnancy on acute lung injury.