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Role of blood cells in ischaemia-reperfusion induced endothelial barrier failure Rodrigues SF; Granger DNCardiovasc Res 2010[Jul]; 87 (2): 291-9Ischaemia and reperfusion (I/R) elicits an acute inflammatory response that is characterized by the recruitment of inflammatory cells, oxidative stress, and endothelial barrier failure. Over the past three decades, much progress has been made in our understanding of the mechanisms that underlie the inflammatory response and microvascular dysfunction associated with I/R. This review is focused on the role of leucocytes (neutrophils and T-lymphocytes) and platelets, and their activation products, as mediators of I/R-induced endothelial barrier failure. The contributions of cytokines, chemokines, and oxidative stress to I/R-induced barrier dysfunction are also discussed. It concludes with an analysis of how risk factors for cardiovascular disease, i.e. hypertension, diabetes, hypercholesterolaemia, and obesity, influence the vascular permeability response to I/R. Areas of uncertainty and controversy in this field of investigation are also identified.|*Capillary Permeability[MESH]|Animals[MESH]|Blood Platelets/immunology/metabolism[MESH]|Body Fluids/*metabolism[MESH]|Endothelium, Vascular/immunology/*metabolism/physiopathology[MESH]|Humans[MESH]|Inflammation Mediators/metabolism[MESH]|Inflammation/blood/physiopathology[MESH]|Microvessels/immunology/*metabolism/physiopathology[MESH]|Neutrophils/immunology/metabolism[MESH]|Reperfusion Injury/*blood/etiology/immunology/physiopathology[MESH]|Risk Factors[MESH]|Signal Transduction[MESH]|T-Lymphocytes/immunology/metabolism[MESH] |
