Expression of ICAM-1 and VCAM-1 on endothelial cells after global cerebral ischemia and reperfusion in the rat

Hypothermic circulatory arrest has been widely adopted in cardiovascular surgery to facilitate correction of congenital and acquired lesions. However, the central nervous system (CNS), is exquisitely sensitive to anoxic insults associated with cerebral ischemia during circulatory arrest. Additional to the abnormalities of the blood flow, metabolism and function of the brain during ischemia and reperfusion, leukocyte-mediated tissue damage will continue despite restoration of blood flow (1 – 3). This may promote the cerebral ischemia/reperfusion injury and contribute to the long-term neurological and neuro-psychological consequences of circulatory arrest (4). ICAM-1 and VCAM-1, the members of supergene family, are inducible ligands expressed on endothelial cells. After exposure to cytokines, they bind to the receptors LFA-1 and VLA-4 on leukocytes. It has become clear that ICAM-1 and VCAM-1 play important roles in leukocyte adherence to endothelium and leukocyte transmigration to inflammation sites (5).