Traumatic brain injury (TBI) is well known to trigger multiple brain parenchymal and vascular responses. The immediate and prolonged opening of blood-brain barrier (BBB) is a hallmark of TBI pathophysiology, and results in extravasation of blood components, including red blood cells, plasma proteins and water (vasogenic edema) [1]. On the other hand, Studies in impact biomechanics have demonstrated a number of brain injury mechanisms [2]. These mechanisms include positive pressures at the impact site, negative pressure at the site opposite of impact. Recently, Hardy et al. demonstrated the presences of transient pressure pulses with impact conditions. Coup pressures measured within a pressurized cadaver head after impact ranged from 34 to 160 kPa, and the contrecoup pressures ranged from −2 to −48 kPa [3]. Pamela et al. tested the effect of overpressure from positive pressure to negative pressure on astrocytes. Pressure wave generated by the barochamber, with high amplitude and short duration in the first pulse [4]. However, there is a lack of information with regards to the effect of impact pressure on endothelial cells in vitro, which are the components of BBB.

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