Diagnosis and therapeutic monitoring of human brain infarcts are largely dependent on imaging techniques such as computed axial tomography and magnetic resonance imaging Yet, the radiological findings, especially contrast enhancement(CE), are not well...
Diagnosis and therapeutic monitoring of human brain infarcts are largely dependent on imaging techniques such as computed axial tomography and magnetic resonance imaging Yet, the radiological findings, especially contrast enhancement(CE), are not well correlated with the histopathological findings of the infarcts. By imaging techniques, CE is observed along the cortical margin of the infarcts, delayed in time after the initial attack Explanation of the CE in terms of histopathological changes is the purpose of this study.
Brain infarction was evoked by injection of homologous blood clots into the right common carotid artery of the rats. Three weeks after the injection, infarcts were examined light and electron microscopically. To confirm the possible increased permeability of vessels, horseradish peroxidase was injected intravenously before sacrifice of some rats. Unaffected brain tissue contralateral to the infarcts was examined for control. The results were as follows.
Capillaries of the normal brain showed endothelial cells connected with tight junctions and approximated intimately to basement membrane on which cytoplasmic processes of the astrocytes mt Pinocytotic vesicles in the endothelial cells were rarely observed Horseradish peroxidase was confined almost to the capillary lumens. In contrast, regenerated capillaries in the infarcts showed endothelial cells with thin cytoplasmic processes protruded into the lumens and many pinmytotic vesicles. Tight junctions and basement membrane were well formed, but astrocytes were not observed Horseradish peroxidase was noted in the pinocytotic vesicles and around the capillaries. The regenerated capillaries were noted almost exclusively along the cortical margin of the infarcts.
From the above results, CE of human brain infarcts along the cortical margin may be explained by the permeable capillaries regenerated at the cortical periphery of the infarcts.