Advances in the vascular pathophysiology of ischemic stroke

The cerebral vascular supply is constructed to protect the cerebral hemisph eres and brainstem from the consequences of blood flow cessation. Reversal of blood flow around local obstructions is a feature of the microvascular b eds of the striatum and cerebral cortex. Cerebral capillaries of these beds consist of endothelial cells, basal lamina, and astrocyte end-feet that si t in close apposition. The interaction of astrocytes with neurons indicates the close relationship, of microvessels to neurons, These relationships ar e altered when blood flow ceases in the supplying artery. Increased endothe lial cell permeability and endocytoses load to edema formation, and matrix degradation is associated with hemorrhage, Autoregulation is lost, Ischemia initiates leukocyte adhesion receptor expression, which is promoted by cyt okine generation from the neuropil and activated monocytes. "Preactivation" may further augment the inflammatory responses to ischemia, The activation of cerebral microvessels by ischemia is heterogeneous, involving alteratio ns in integrin-matrix interactions, leukocyte-endothelial cell adhesion, pe rmeability changes, and the "no-reflow'' phenomenon due to platelet activat ion, fibrin formation, and leukocyte adhesion. Ischemia produces swelling o f the microvascular endothelium, and rapid detachment and swelling of the a strocyte end-feet. Ischemic injury targets the microvasculature, where the inflammatory responses are initiated and contribute to tissue injury. (C) 2 000 Elsevier Science Ltd. All rights reserved.