Hypothermia reversibly inhibits endothelial cell expression of E-selectin and tissue factor

Hypothermia frequently accompanies cardiopulmonary bypass (CPB) and myocardial protection strategies during cardiac surgery. With CPB, the blood/artificial surface interface activates components of the humoral and cellular inflammatory cascades and may contribute to postoperative end organ dysfunction including the heart or multiple other organ systems. The endothelial cell (EC) monolayer normally mediates components of solute transport, vasomotor function, coagulation, cell differentiation/growth, and immune/inflammatory processes. E-selectin is a vascular adhesion molecule that mediates neutrophil adherence and that is inducible in ECs by inflammatory mediators such as cytokines. Tissue factor (TF) is similarly an inducible procoagulant factor in ECs that contributes to thrombosis. The induction, transcription, and expression of both molecules were studied in cultured human umbilical vein cells at normothermic (37 degrees), hypothermic (25 degrees), and rewarmed (37 degrees) conditions after stimulation with the cytokines tumor necrosis factor alpha and interleukin-1. Hypothermia reversibly inhibits the transcription and expression but not the induction of both E-selectin and TF.