Blood–brain barrier damage is an early event in porcine endotoxemic shock

Background

Cerebral dysfunction is frequently seen in septic shock and correlates to outcome. The pathogenesis of the cerebral dysfunction is unknown. We decided to study the effects of experimental septic shock on cerebral damage, as evaluated by the serum levels of S100B, a well-established marker for brain and blood–brain barrier damage.

Materials and methods

Endotoxemic shock was induced in 10 anesthetized domestic piglets by an infusion of Escherichia coli endotoxin. Blood samples for hemoglobin and S100 B measurements were taken at baseline and repeated hourly. After 6 hours, the piglets were sacrificed. S-100B was measured by sandwich ELISA.

Results

All animals had very low S100B values at baseline. There were significant increases in S-100B at 1–5 hours in comparison with the baseline values. The increases in S100B were most expressed at 3 hours, at which time point the levels were increased up to ninefold (P < 0.05). Changes in hemoglobin levels reflected an increased vascular permeability during endotoxemic challenge. The magnitude of the increase in hemoglobin was considerably less expressed than those of S100B.

Conclusion

Anesthesia does not per se induce these changes in our pig model. The increase of S100B found in this study thus shows that there is minor blood–brain barrier damage occurring already during the first hours of porcine endotoxemic shock. Serum samples of S100B may be an alternative to cerebrospinal fluids in evaluating blood–brain barrier damage. Such sampling may, in certain selected cases, even turn out to be of value in clinical practice, as spinal puncture is hazardous to perform in patients with coagulation disturbances (e.g. in septic shock).

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