The brain is a major source of S100 increase in porcine endotoxemic shock

Introduction

Cerebral dysfunction frequently complicates septic shock. A marker of cerebral dysfunction could be of significant value in managing sedated septic patients. Plasma S100 (S100B) proteins increase in sepsis. S100B is present in the brain, but also in other tissues. To date, the source of this protein has not been investigated in sepsis. The aim of this study is to determine whether the brain is the source of S100B in an experimental sepsis model.

Methods

Twenty-seven pigs were anesthetized and randomized to either infusion of endotoxin at the rate of 1 μg/kg/hour (n = 19) or saline (n = 8). Catheters were inserted into a cervical artery and the superior sagittal sinus. Blood samples were collected from both sites and physiological data were registered before the start of the endotoxin infusion and hourly. After 6 hours, the animals were terminated and brain tissue samples were taken from the left hemisphere. S100B in plasma was measured by ELISA. Brain tissue samples were stained with biotinylated S100B antibodies.

Results

S100B levels increased in plasma and expression of S100B in cerebral tissue was higher in endotoxemic animals compared with controls. Statistically higher sinus versus arterial S100B concentration was only found at 2 hours in the endotoxemic animals (Figure 1).

Figure 1

Brain sinoarterial S100B concentration differences over time. Mean/SE. *P < 0.05.

Conclusion

Although other sources exist, the brain is a major source of S100B in endotoxemia, making it a potential marker of cerebral dysfunction in septic shock.