Morphological features in human cortical brain microvessels after head injury: A three‐dimensional and immunocytochemical study

Abstract

We studied the morphology of cortical microvessels in the brains of 10 patients who had died after receiving a traumatic head injury (THI). Scanning electron microscopy (SEM) of vascular corrosion casts, confocal microscopy of histological sections after immunocytochemistry, and detection of apoptosis by terminal dUTP nick end labeling (TUNEL) were used. Microvascular casts showed an angioarchitectonic distribution that was defined as normal according to results obtained in a previous, nontraumatic series of subjects. However, when we compared them with previous works, the cast surface of some of the microvessels showed three types of morphological alterations: longitudinal folds, sunken surfaces with craters, and a significant flattening with reduction of lumen. The vessels that were primarily affected were the arterioles and capillaries of the middle and deep cortical vascular zones. Immunostaining with the monoclonal antibody MAS-336 against endothelial cells also showed the presence of longitudinal folds with a thinning of the vascular lumen, cytoplasmic round bodies, and a thickening of the endothelial cell membrane. The TUNEL technique revealed a positive staining of some endothelial cells.The structural alterations we observed indicate that microvessels undergo endothelial cell damage after THI. We suggest that this kind of lesion and the secondary functional injury to the blood-brain barrier (BBB) could play an important role in the development of the secondary lesions that these patients show in the subacute phase. Anat Rec Part A 273A: 583-593, 2003.

Blood-Brain Barrier Disruption Is an Early Event That May Persist for Many Years After Traumatic Brain Injury in Humans

“…As regards possible structural correlates of this acute BBB disruption, ultrastructural studies in animal models of TBI have identified a variety of alterations in vascular endothelia in the Page 14 of 22 acute phase following injury, including the formation of vacuoles, craters and microvilli (47,(57)(58)(59) some of which were later identified in human TBI (60,61). These very rapid changes in vascular structure and function have been attributed to a range of mechanisms such as direct perturbation of the vessels by mechanical forces, including the immediate disruption of vascular endothelial cells.…”

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“…NVU is at the basis of neurovascular coupling, which allows cerebral blood flow to local regulation according to neuronal Traumatic Brain Injury -Pathobiology, Advanced Diagnostics and Acute Managementactivity in specific areas of the brain [34]. TBI may cause mechanical deformation and damage to the entire NVU [20,35,36], compromising barrier integrity and leading to dysautoregulation of brain vessels and BBB disruption. In this context, brain edema may occur and result in increased ICP and decreased cerebral perfusion [37].…”

The Blood-Brain Barrier in Epilepsy

“…The blood-brain barrier is a network of brain capillaries (microvessels). With a diameter of 3-7 μm, brain capillaries are the smallest vessels of the vascular system (Figure 2A) (Rodriguez-Baeza et al, 2003). The microvasculature in the human brain is comprised of about 100 billion capillaries forming a highly branched vascular network www.intechopen.com…”

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