Trauma - after hemorrhagic shock in immune cell function suppression and countermeasures.docVIP
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Trauma - after hemorrhagic shock in immune cell function suppression and countermeasures
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Trauma - after hemorrhagic shock in immune cell function suppression and countermeasures
Trauma can lead to excessive inflammatory response and significant inhibition of cellular immune function, surgical or trauma patients in easy-to-concurrent infections and / or multi-organ failure, multiple organ failure has become the leading cause of death in patients after surgery. The normal immune response depends on the Th1/Th2 response to the full, complete, single-nucleated cells-T cell interactions and the appropriate cytokines. In this paper, overview of animal models of traumatic shock and major abdominal surgery after massive loss of blood macrophages and T cell function changes.
1. Trauma and blood loss after the cardiovascular response.
After the trauma and blood loss, cardiac output and organ blood flow changes, so that tissue perfusion and oxygen supply decrease, leading to cellular hypoxia and organ damage or even death. Vascular endothelial cells to release NO, the control of a key factor in vascular smooth muscle tension. Trauma and blood loss after vascular endothelial function was inhibited, endothelium-derived NO release to reduce, so that vasodilator dysfunction or even disappear, an increase of platelet aggregation and neutrophil invasion increased; capillaries also appeared these reactions, increased microvascular permeability endothelial integrity of the damage, there capillary leakage, adhesion molecules such as intercellular adhesion molecule (ICAM) -1, vascular cell adhesion molecule (VCAM) -1, P-selectin and E-selectin expression, etc. increased, in order to initiate the inflammatory response, which led to injury - after hemorrhagic shock immunosuppression. Have confirmed that exogenous antigen endocytosis by macrophages, and lysis of small antigenic peptides, these small peptides by compression on the cell surface MHC-II molecules presented to CD4 T cells, antigen-presenting require cell surf
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