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starch/inflamación
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Early treatment with hydroxyethyl starch 130/0.4 causes greater inhibition of pulmonary capillary leakage and inflammatory response than treatment instituted later in sepsis induced by cecal ligation and puncture in rats.
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This study investigated the temporal profile of effects of hydroxyethyl starch (HES) 130/0.4 on pulmonary capillary leakage in a rat sepsis model induced by cecal ligation and puncture (CLP). Arterial blood pressure and heart rate were monitored during the experiment. Pulmonary capillary leakage was
Dietary resistant starch and chronic inflammatory bowel diseases.
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These studies were performed to test the benefit of resistant starch on ulcerative colitis via prebiotic and butyrate effects. Butyrate, propionate, and acetate are produced in the colon of mammals as a result of microbial fermentation of resistant starch and other dietary fibers. Butyrate plays an
Evaluation of the potential of starch-based biodegradable polymers in the activation of human inflammatory cells.
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The inflammatory response resulting from the implantation of a medical device may compromise its performance and efficiency leading, in certain cases, to the failure of the implant. Thus, the assessment of the behavior of inflammatory cells in vitro, constitutes a key feature in the evaluation of
Effects of colloid solutions on ischemia-reperfusion-induced periosteal microcirculatory and inflammatory reactions: comparison of dextran, gelatin, and hydroxyethyl starch.
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OBJECTIVE
To compare the microhemodynamics and possible anti-inflammatory reactions of colloid resuscitation with 4% gelatin, 6% dextran, or 6% hydroxyethyl starch 130/0.4 solutions.
METHODS
A randomized control in vivo animal study in a university research laboratory.
METHODS
Adult male Wistar rats
Immune and inflammatory role of hydroxyethyl starch 130/0.4 and fluid gelatin in patients undergoing coronary surgery.
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OBJECTIVE
Compare the effects on inflammatory (TNF-α, IL-6, IL-8 and IL-10) and immunologic (CD3(+), CD4(+), CD8(+), CD11b(+), CD16(+)/56(+) T cells and total lymphocyte concentration) variables of hydroxyethyl starch 130/0.4, 4% modified fluid gelatin, or crystalloid when used as volume replacement
Hydroxyethyl starch inhibits NF-kappaB activation and prevents the expression of inflammatory mediators in endotoxic rats.
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Hydroxyethyl starch (HES) has been shown to be beneficial in several inflammatory situations, but the mechanisms are unclear. The present study tested the hypothesis that HES has effects on nuclear factor kappa B (NF-kappaB) activation and the expression of inflammatory mediators induced by
Hydroxyethyl starch 130/0.4 exerts its anti-inflammatory effect in endotoxemic rats by inhibiting the TLR4/NF-kappaB signaling pathway.
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Previous studies demonstrated that hydroxyethyl starch (HES) down-regulates the inflammatory response, but the mechanism is controversial. The present study measured the effects of HES130/0.4 on plasma proinflammatory cytokines levels and the Toll-like receptor-4 (TLR4)/nuclear factor-kappa B
Mechanisms of the anti-inflammatory effects of hydroxyethyl starch demonstrated in a flow-based model of neutrophil recruitment by endothelial cells.
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OBJECTIVE
To determine whether plasma volume expander hydroxyethyl starch (HES) may protect against reperfusion injury through an ability to reduce neutrophil recruitment.
METHODS
An in vitro study using paired comparisons of adhesion of flowing neutrophils.
METHODS
A collaboration between clinical
Sweet potato [Ipomoea batatas (L.) Lam. "Tainong 57"] starch improves insulin sensitivity in high-fructose diet-fed rats by ameliorating adipocytokine levels, pro-inflammatory status, and insulin signaling.
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The aim of this study was to investigate the effects of low-glycemic index (GI) sweet potato starch on adipocytokines, pro-inflammatory status, and insulin signaling in the high-fructose diet-induced insulin-resistant rat. We randomly divided 24 insulin-resistant rats and 16 normal rats into two
Effects of synthetic colloids on oxidative stress and inflammatory response in hemorrhagic shock: comparison of hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, and succinylated gelatin.
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BACKGROUND
This study compared the effects of hydroxyethyl starch 130/0.4, hydroxyethyl starch 200/0.5, and succinylated gelatin on oxidative stress and the inflammatory response in a rodent hemorrhagic shock model.
METHODS
Sodium pentobarbital-anesthetized adult male Wistar rats (200 g to 220 g)
Effects of resistant starch interventions on circulating inflammatory biomarkers: a systematic review and meta-analysis of randomized controlled trials.
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The effects of hydroxyethyl starch compared with gelofusine on activated endothelium and the systemic inflammatory response following aortic aneurysm repair.
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OBJECTIVE
To investigate the effect of HES, used as a plasma volume expander, on endothelial cell activation induced by ischaemia-reperfusion in humans.
METHODS
Forty patients undergoing elective infrarenal aneurysm repair were randomised to receive either gelatine or hydroxyethyl starch solution as
Hydroxyethyl starch resuscitation downregulate pro-inflammatory cytokines in the early phase of severe acute pancreatitis: A retrospective study.
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In the present study, we investigated the effects of hydroxyethyl starch (HES) 130/0.4 on serum pro-inflammatory variables, immunologic variables, fluid balance (FB)-negative(-) rate and renal function in severe acute pancreatitis (SAP) patients. From October, 2007 to November, 2008, a total of 120
Protective roles of hydroxyethyl starch 130/0.4 in intestinal inflammatory response and survival in rats challenged with polymicrobial sepsis.
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BACKGROUND
The gut is considered an important target organ of injury after severe insult such as sepsis, trauma and shock. Hydroxyethyl starch (HES) 130/0.4 has been developed to improve the pharmacokinetics of current medium molecular weight HES solutions. We investigated the protective effects of
Hydroxyethyl starch 130/0.4 prevents the early pulmonary inflammatory response and oxidative stress after hemorrhagic shock and resuscitation in rats.
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BACKGROUND
This study was designed to determine the effects of various resuscitation fluids on pulmonary capillary leakage and pulmonary edema after HS and fluid resuscitation (HS/R) and to determine whether an antiinflammatory or antioxidative mechanism was involved.
METHODS
We induced HS by
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