starch/inflammation

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

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

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

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

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 (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

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

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

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

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)

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

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

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

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