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ABS, including the potential of hydrogen (pH), partial pressure of carbon dioxide in arterial blood (PaCO2), partial pressure of oxygen in arterial blood (PaO2), and base excess (BE), was measured in postpartum rats with BMODS (Table 2).
The mRNA expression of IFN-[gamma] and IL-4 in the lung tissue of the S+C group was significantly (P < 0.05) higher than in that of the Sham group, indicating that an inflammatory response was elicited in postpartum rats with BMODS. The IFN-[gamma], IL-4, and IFN-[gamma]/IL-4 mRNA ratios were significantly lower in S+C+D2.5 and S+C+D5.0 than in S+C, indicating reduced IFN-[gamma] and IL-4 release upon DEX administration during postpartum BMODS.
However, the effects of DEX on BMODS have not yet been evaluated.
A small number of animal models are available for studying the pathogenesis of BMODS, but treatments have been largely unsuccessful, especially in patients with postpartum BMODS.
Therefore IFN-[gamma] and IL-4 are the best respective markers for Th1 and Th2 cells, and they were chosen to evaluate the changes in immune function in postpartum rats with BMODS in the present study.
This finding may provide a basis for additional management options for patients with BMODS. In current practice, BMODS patients are treated with mechanical approaches to prevent lung injury, including reducing the tidal volume of mechanical ventilation and positive pressure ventilation at the end of breath [35].
In summary, the present study demonstrated that DEX administration reduced IFN-[gamma] and IL-4 release and decreased lung injury during postpartum BMODS. It is possible that DEX administration decreased inflammatory cytokine production in BMODS by inhibiting inflammation and free radical release by leukocytes independent of the DEX dose.