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Hypothemia Reversibly Inhibits Endothelial Cell Expression of E‐Selectin and Tissue Factor
Author(s) -
Johnson Marion,
Haddix Terri,
Pohlman Timothy,
Verrier Edward D.
Publication year - 1995
Publication title -
journal of cardiac surgery
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.428
H-Index - 58
eISSN - 1540-8191
pISSN - 0886-0440
DOI - 10.1111/j.1540-8191.1995.tb00673.x
Subject(s) - tissue factor , medicine , umbilical vein , cell adhesion molecule , microbiology and biotechnology , selectin , endothelial stem cell , tumor necrosis factor alpha , cardiopulmonary bypass , platelet , immune system , chemokine , immunology , coagulation , biology , in vitro , biochemistry
A bstract 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°), hypothermic (25°), and rewarmed (37°) 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.