P-Selectin and Intercellular Adhesion Molecule-1 Expression After Focal Brain Ischemia and Reperfusion

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Background and Purpose

Polymorphonuclear leukocytes have been implicated in the development of the “no-reflow” phenomenon after focal cerebral ischemia and reperfusion. To further understand the role of granulocytes in microvascular occlusions, the responses of the granulocyte-endothelial cell adhesion molecules P-selectin and intercellular adhesion molecule-1 during middle cerebral artery ischemia and reperfusion were examined in a primate model.


Twelve adolescent male baboons were used for 2-hour middle cerebral artery occlusion (n=3) or for 3-hour occlusion with 1-hour (n=3), 4-hour (n=3), and 24-hour (n=3) reperfusion, and three separate unoperated primates served as controls. A quantitative immunohistochemical study of the microvascular distribution of P-selectin and intercellular adhesion molecule-1 was performed using 10-μm frozen sections from basal ganglia analyzed with computerized light microscopy video imaging.


Significant (P <.05) persistent upregulation of P-selectin (beginning during ischemia) and transient upregulation of intercellular adhesion molecule-1 (at 1 and 4 hours of reperfusion) were observed on endothelium of selected post-capillary microvessels of the ischemic lenticulostriate artery territory. Platelet accumulation also occurred in this territory and was responsible for a significant proportion of the nonendothelial P-selectin signal at 24 hours after reperfusion.


Focal cerebral ischemia/reperfusion stimulates endothelial P-selectin and intercellular adhesion molecule-1 expression in brain microvessels in the ischemic zone, which may contribute to enhanced leukocyte adherence and persistent activation.

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