Fig. 8

A Effects of glymphatics, BBB disruption, and the trauma index on venous blood S100B. Note that activating release from astrocytes (Trauma_Index) prevents return of S100B to pre-BBBD values, suggesting that parenchymal S100B is involved in the half-life of S100B. B1 and B2 “Filling” of empty organs (S100B set at 0 in adipose, muscle, and gut tissues) after a 100-h simulation with glymphatic communication between brain interstitial S100B and periphery. B2 Changes in venous S100B in empty or full organs in the presence or absence of glymphatic contribution. When no S100B is available (blue line) venous levels are clamped at 0. When S100B in peripheral organs and glymphatic communication are present, a slight transient increase in venous S100B is seen. This is amplified by “opening” the BBB and establishment of a communication between glial cells reservoir and brain interstitial S100B. The data show that peripheral levels in organs can derive from brain reservoirs. C1 Simulation identical to A but at a lower concentration of brain interstitial S100B. C2 Simulation as in B1 but with low levels of brain interstitial S100B. D Time course of S100B changes in various compartments under normal (D1), BBB disruption (D2), and trauma (D3)