Abstract

Nitric oxide (NO) plays a key role in innate immune system controlling microbial infection; however, during septic shock its exacerbate formation is associated with several deleterious complications. Cholecystokinin (CCK) was first described as a gastrointestinal hormone, but immune cells express their receptor, suggesting a possible involvement of this hormone in modulation of inflammatory response. Our aim was to evaluate the role of CCK on NO production during endotoxemia in rats as well as lipopolysaccharide (LPS)-stimulated macrophages.

Highlights

  • In 2002, the Surviving Sepsis Campaign defined a strategy that aimed to reduce the high mortality due to sepsis

  • Endogenous respiration of intact platelets suspended in their own plasma or PBS glucose was determined and, in order to investigate the activity of individual complexes of the respiratory system, platelets were permeabilized with digitonin and stimulated with complex-specific substrates and inhibitors

  • For example at 5 μg/ml LPS, the expression of GIPR was reduced to 86% and INSR 72% of control in U937: while in HUH7 cells at 1 μg/ml LPS, the GIPR expression was decreased to 63%, GLP-1R 95% and INSR 89% compared with control (P

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Summary

Introduction

In 2002, the Surviving Sepsis Campaign defined a strategy that aimed to reduce the high mortality due to sepsis. Patients admitted to ICUs with severe sepsis have a 39.8% risk of death [2], and for each hour delay in antibiotic administration, a 7.6% increase in mortality [3]. The objective of the present study was to evaluate the impact of early fluid resuscitation on serial TNFα and IL-6 levels and its association with mortality in severe sepsis. Our laboratory has demonstrated in preliminary clinical studies among the various biomarkers of endothelial dysfunction that blood levels of endocan (ESM-1), a pulmonary vascular endothelial cell-specific molecule participating in the control of endothelial–leukocyte interactions, are associated with the severity and evolution of septic states. The objective, of our study was to predict the development of organ failure at 24 hours using only the data available from the first 4 hours post inoculation Methods This pneumonia-sepsis model included 19 sheep with ALI. The sera were analyzed through serological (IgM and IgG specific ELISA) and molecular (gel-based and real-time RT-PCR) testing

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