Abstract
BackgroundIntracranial pressure changes during head impact cause brain injuries such as vasogenic edema and cerebral contusion. However, the influence of impulsive pressure on endothelial function has not yet been fully studied in vitro. In this study, we developed a pressure loading device that produced positive and negative pressures by modifying an in vitro fluid percussion model and examined the effects of the amplitude and duration of the pressures on endothelial permeability.MethodsHuman umbilical vein endothelial cells were subjected to three types of positive pressure (average amplitude/average duration of 352 kPa/23 ms, 73 kPa/27 ms, and 70 kPa/44 ms) and three types of negative pressure (−72 kPa/41 ms, −67 kPa/104 ms, and −91 kPa/108 ms), and the transendothelial electrical resistance (TEER) was measured between 15 min and 24 h after pressure loading for quantifying the formation of an integral monolayer of endothelial cells. After loading, vascular endothelial- (VE-) cadherin, an endothelium-specific cell-cell adhesion molecule involved in endothelial barrier function, was stained and observed using fluorescence microscopy.ResultsThe pressure loading device could produce positive pressure pulses with amplitudes of 53–1348 kPa and durations of 9–29.1 ms and negative pressure pulses with amplitudes of −52–−93 kPa and durations of 42.9–179.5 ms. The impulsive pressure reduced the TEER associated with the change in VE-cadherin localization. Additionally, TEER decreased considerably at 15 min and 6 h post-loading, with these changes being significant in positive pressure with larger amplitude and shorter duration and in all types of negative pressures compared to pre-loading.ConclusionsThe changes in intracranial pressure during head impact impair endothelial barrier function by the disruption of the integrity of endothelial cell-cell junctions, and the degree of increase in endothelial permeability depends on the amplitude, duration, and direction (compressive and tensile) of the impulsive pressure.
Highlights
Intracranial pressure changes during head impact cause brain injuries such as vasogenic edema and cerebral contusion
Studies of experimental animals using a fluid percussion injury model and controlled cortical impact model have shown that cerebral vascular dysfunction such as morphologic damage to endothelial cells and increased permeability of blood-brain barrier (BBB) forms a physical barrier to filter blood-borne substances between the blood and the brain parenchyma [12]; the effects of pressure on cultured cells have been poorly studied relative to the effects of deformation, and few studies have focused on the endothelial cells of brain microvessels [11,13,14], which define one component of BBB, compared to central nervous system (CNS) cells such as neurons, astrocytes, and glial cells
We examined the effects of the amplitude and duration of positive and negative pressures on the capillary-like structure and endothelial permeability using a pressure loading device developed by modifying an in vitro fluid percussion model
Summary
Intracranial pressure changes during head impact cause brain injuries such as vasogenic edema and cerebral contusion. Animal studies of head impact have shown that the transient increase in intracranial pressure causes brain haemorrhage and cerebral concussion [3,4]. Studies of experimental animals using a fluid percussion injury model and controlled cortical impact model have shown that cerebral vascular dysfunction such as morphologic damage to endothelial cells and increased permeability of blood-brain barrier (BBB) forms a physical barrier to filter blood-borne substances between the blood and the brain parenchyma [12]; the effects of pressure on cultured cells have been poorly studied relative to the effects of deformation, and few studies have focused on the endothelial cells of brain microvessels [11,13,14], which define one component of BBB, compared to central nervous system (CNS) cells such as neurons, astrocytes, and glial cells. The direct influence of impulsive pressure during head impact on the structure and function of endothelial cells in vitro has not yet been fully studied
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