Neovasculature and blood-brain barrier in ischemic brain infarct.
The cellular events occurring in ischemic brain infarcts of 1 day to 8 weeks duration were investigated. The material consisted of 17 human postmortem brains with anemic infarcts caused by occlusive vascular diseases. Using antiserum against human plasma albumin as a marker for the breakdown of blood-brain barrier and ammoniacal silver nitrate stain to demonstrate the vasculature, the onset and distribution of the extravasated plasma protein was compared with histological changes in the blood vessels. It was observed that extravasation occurred in several separate regions of the infarct during different time periods. During the first few days, plasma proteins exudated from the vessels located at the marginal zone surrounding the infarct. This was followed by a prolonged phase of intense extravasation that coincided with the production of new capillaries originating from the blood vessels at the margin of the infarct and from pial vessels. It is postulated that the actively proliferative and migratory activities of the endothelial cells and pericytes in the neovasculature may be responsible for the extravasation which is reflected in the contrast enhancement of the infarct observed clinically during the recovery phase.
D001812:Blood-Brain Barrier; D001921:Brain / Q000098:blood supply / Q000378:metabolism / Q000473:pathology*; D002544:Cerebral Infarction / Q000473:pathology*; D006801:Humans; D007142:Immunoglobulin gamma-Chains / Q000032:analysis; D007150:Immunohistochemistry; D012709:Serum Albumin / Q000032:analysis; D013997:Time Factors
D007142:Immunoglobulin gamma-Chains; D012709:Serum Albumin