The Journal of surgical research
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Burn injury delays allograft rejection and impairs the host defense against infection. These functions are mediated via the cytotoxic T-lymphocyte (CTL) response. The CTL response is divided into antigen recognition/processing and effector phases. Presensitization allows selective analysis of changes, induced by burn injury, in the effector limb of the CTL response in relation to time and burn size. ⋯ Burn injury impairs the effector limb of the CTL response as a function of burn size in the immediate postburn period. CTL activity returns to baseline within 7-10 days postburn and has a rebound increase by Day 14. Early CTL suppression, after burn injury, may be due to a decrease in the T-helper subpopulation. The late increase in cytotoxicity may be secondary to an increase in the effector CTL population in the late postburn period. Burn injury causes a T-helper-2 phenotype as demonstrated by depressed IL-2 and IFN-gamma production and increased IL-5 production.
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To identify vascular beds where endogenous adenosine plays a significant role as a mediator of resting perfusion alterations associated with sepsis, we tested the hypothesis that adenosine receptor blockade would cause differential regional increases in vascular resistance during intraperitoneal (ip) sepsis in the rat. ⋯ These data suggest that adenosine receptor-mediated actions during sepsis affect vascular beds selectively and indicate a significant role for adenosine in resting perfusion redistribution in sepsis.
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Endothelial cells (EC) are important for regulating the hemostatic balance of prothrombotic and antithrombotic activities. Proinflammatory cytokines such as tumor necrosis factor-alpha (TNFalpha) play an important role in the regulation of EC and also regulate the production of plasminogen activator inhibitor type 1 (PAI-1), which is an EC-producing factor with the inhibitory activity of fibrinolysis, and the expression of intercellular adhesion molecule-1 (ICAM-1), which is an adhesion molecule that plays an important role in inflammation. Protease inhibitors such as gabexate mesilate (GM) and ulinastatin (UTI) have been shown to improve the microcirculatory environment and reduce tissue damage, but the mechanism for this has yet to be fully elucidated. We investigated the effect of GM or UTI on EC regarding PAI-1 synthesis and ICAM-1 expression. ⋯ These data suggest that GM may thus provide a beneficial effect which improves the microcirculatory environment and prevents tissue damage by inhibiting the activation of the vascular EC themselves.
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Comparative Study
Resuscitation with hypertonic saline dextran reduces endothelial cell swelling and improves hepatic microvascular perfusion and function after hemorrhagic shock.
Hemorrhagic shock severely compromises hepatic microcirculation and function with tendency to promote hepatic insufficiency and multiple organ failure. ⋯ Reduction of mean endothelial cell thickness after HSD is very likely the mechanism for the amelioration of sinusoidal perfusion, resulting in a significant improvement of hepatic energetic status and excretory function.
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The purpose of this work was to determine the effects of hypoxemia on systemic hemodynamic variables and regional conduit arterial blood flows in neonatal piglets. ⋯ The physiologic mechanisms responsible for neonatal mesenteric vasoactive responsiveness are present in conduit and in nutrient vessels well prior to birth and can be activated by a significant perturbation. These observations are germane insofar as they provide a stable, age-matched acute animal model to study neonatal intestinal ischemic diseases, including necrotizing enterocolitis.