Formation of transendothelial channels in traumatic human brain edema.

The formation of incomplete transendothelial channels is reported in four cases of traumatic human brain injury complicated with subdural or epidural hematoma or hygroma. Such structures were observed coexisting with increased transendothelial vacuolar and vesicular transport. They appeared in the following manners: as electron lucent corridors formed by deep invaginations of luminal endothelial plasma membranes, as chained spheroidal or elongated vacuoles connected with the luminal and abluminal endothelial membranes, as a result of a combined process of membrane fusion and fission, as a large protein containing vacuole or a micropinocytotic vesicle occupying the entire width of peripheral endothelial cytoplasm, as abluminal profiles of dilated basement membrane expansions, extending their course to the vicinity of endothelial luminal plasma membrane. The endothelial junctions appeared intact in most cases. The transendothelial channels apparently represent a transcytosis response to the traumatic brain injury. They may provide specific cytoplasmic corridors of facilitated transport for edema formation, which incorporate the intraluminal capillary content, ferry it across the peripheral zone of endothelial cytoplasm and empty it at the abluminal surface, into the surrounding basement membrane, from where it floods the intercellular spaces of neighbouring neuropile. The albuminal transendothelial channels, formed by the dilated basement membrane bifurcations, might be a reverse shuttle for endogeneous substances moving from parenchymal clefts to blood as a capillary mechanism of edema resolution.