Increased maternal/fetal blood S100B levels following systemic endotoxin administration and periventricular white matter injury in preterm fetal sheep

Objective. Intrauterine infection is suggested to cause perinatal brain white matter injury. Ill the current study, we evaluated whether S100B, a brain damage marker, may, be also assessed in maternal bloodstream after white matter injury induced by fetal intravenous application of lypopolisaccharide (LPS) endotoxin. Methods. Fourteen fetal sheeps were chronically catheterized at a mean gestational age of 907 days. Three days after surgery, fetuses (n = 7) received 500 rig of LPS or 2 mL 0.9% saline (n = 7) intravenously (IV). Lypopolisaccharide ail placebo groups were monitored by continuous hemodynamic data recordings and at 6 predetermined time points (control value; 3, 6, 24, 48, and 72 hours after LPS/placebo administration) blood was drawn for laboratory parameters and S100B assessment. Brain damage was evaluated by light microscopy after Kluver-Barrera staining. Selected areas of the periventricular white matter were also examined by electron microscopy. Results. White matter injury was detected ill all LPS-treated fetuses, whereas no abnormalities were seen ill control animals or ill LPS-treated mothers. Maternal and fetal S100B protein levels were significantly higher ill tire LPS group than ill the control group at all monitoring tune points (P < .009). The highest fetal-maternal S100B levels were observed at 3-hour tune-point (P < .001). Conclusions. We found that S100B protein is increased ill the maternal district ill presence of fetal periventricular brain white matter injury induced by endotoxin. Tire present data offer additional support for S100B assessment ill the maternal circulation ill pregnancies complicated by intrauterine infection at risk of white matter injure