Increased vesicular and vacuolar transport in traumatic human brain edema. A combined electron microscopic study and theoretical approach.

Twelve cortical biopsies obtained from patients with traumatic brain injury, some complicated with subdural or epidural hematoma or hygroma, have been analyzed. The endothelial vacuolar and vesicular transports have been studied in order to establish their probable role in both edema formation and edema resolution. Normal or 'non-activated' and 'activated' capillaries were found. The activated capillaries showed predominantly enhanced abluminally orientated vesicular transport by means of small, medium and large uncoated and coated vesicles as well as the presence of endothelial tubular structures. Activation of the endothelial nuclear zone and vesicles internalizing to the hypertrophic Golgi complex, lysosomes and multivesicular bodies were observed. Vacuolar transport was predominant. In brain injuries of long evolution time, a wide spectrum of endothelial cell mechanisms was observed increasing the vesicular and vacuolar transport. These mechanisms were deep invaginations of luminal surface, large coated vesicles, tubular structures and transient and incomplete transendothelial channels formed either by chained plasmalemmal vesicles or elongated protein-containing vacuoles. Uncoated vesicles were seen surrounding lysosomes. Most endothelial junctions were apparently intact. The present results suggest that vesicular transport might be discriminated between abluminally orientated or transendothelial transport (edema formation) and intraendothelial transport (edema resolution) directed towards cell organelles. The transendothelial passage via large vacuoles seems to be caused by macromolecular transport.