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This technique may be useful in the prenatal diagnosis of conotruncal anomalies and in the assessment of the spatial relationships of abnormal vascular connections in the upper mediastinum. P01.34Maternal lipopolysaccharide depresses fetal cardiovascular function in mouse S. Rounioja, J. Räsänen, H. Autio-Harmainen, M. Ojaniemi, V. Glumoff, K. Mäkikallio, M. Hallman University of Oulu, FinlandBackground: Intra-amniotic lipopolysaccharide (LPS) causes a fetal inflammatory response and cardiac dysfunction in mice. We hypothesized that the placenta serves as a barrier against bacterial toxins delaying the onset of a fetal inflammatory response and cardiac failure. Methods: At 14-15 days of gestation DBA strain mice were randomized to receive LPS (∼ 70 µg) or vehicle intraperitoneally. Doppler ultrasonography of fetal cardiovascular hemodynamics was performed before and six hours after LPS. The expression and production of cytokines and other inflammatory mediators were determined using ribonuclease protection assay and cytometric bead array. Histopathology and immunostaining of toll-like receptor (TLR) in placenta were carried out. Results: Six hours after LPS injection, there was no evidence of stasis in maternal lung or liver, although tumor necrosis factoralpha (TNF-á) and interleukin (IL)-6 were increased in serum (p < 0.05). In contrast, placenta showed severe dilatation and stasis most distinctly in maternal vessels. The expression of TNF-á, IL-1á and IL-6 (p < 0.05) increased in placenta, whereas no inflammatory activation was evident in fetal tissues, and amniotic fluid revealed no increase in cytokines. The expression of TLR2 (p < 0.05) was increased in labyrinthine macrophages, which could serve as target for LPS. The fetal cardiac outflow mean velocity, was lowered (p < 0.005) in the LPS group. The pulsatility indices (PI) of the umbilical artery and the descending aorta and the PI for veins from the ductus venosus were higher after LPS. In the LPS group 65% of the fetuses had atrioventricular valve regurgitation, compared to only 4% in the vehicle group. Conclusions: Maternally administered LPS acutely induced cytokine expressions in placental tissue with histologic lesions. Inflammatory response was not evident in the fetal compartment. However, placental congestion increased the cardiac afterload, leading to fetal cardiovascular dysfunction.