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      Slight increase of serum S-100B during porcine endotoxemic shock may indicate blood-brain barrier damage.

      Anesthesia and Analgesia
      Animals, Biological Markers, Blood-Brain Barrier, physiopathology, Endotoxemia, blood, Female, Hemoglobins, analysis, Male, Nerve Growth Factors, S100 Calcium Binding Protein beta Subunit, S100 Proteins, Shock, Septic, Swine

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          Abstract

          Septic shock is a condition that affects many organs, but little is known about the effects on the central nervous system. S-100B, an acidic low molecular weight protein, has attracted considerable interest as a marker for brain damage and disintegration of the blood-brain barrier. It is released into the cerebrospinal fluid and blood from brain tissue after brain damage. We studied S-100B in a porcine model of endotoxemic shock that resembles human Gram-negative septic shock. Ten piglets received IV endotoxin, and plasma samples were collected before the endotoxin infusion and each hour (1-6 h) during the endotoxin infusion. S-100B was measured by sandwich enzyme-linked immunosorbent assay. Low levels of plasma S-100B were detected, but there was a significant increase in S-100B during Hours 1-5 in comparison with the 0 values. We determined that endotoxemia causes a very small but significant increase in the levels of the widely used brain damage marker serum S-100B. However, it cannot be excluded that the increase in S-100B could be caused by release from organs other than the brain.

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