Sepsis Clinical Trial
Official title:
The Role of Angiopoietin, Angiopoietin Receptor Tie-2, and Vascular Endothelial Growth Factor in Sepsis-Induced Multi-Organ Dysfunction Syndrome
This study is designated to determine serum concentrations of inflammatory mediators Ang-1, Ang-2, Ang-1/Ang-2 ratio, and Tie-2 in patients with sepsis-induced MODS and to investigate the association among increased permeability, inflammatory mediators, and these serum mediators in development of organ failure.
Multiple Organ Dysfunction Syndrome (MODS) frequently leads to death in patients with
sepsis. Our previous work has demonstrated that endothelial injury is closely associated
with MODS development and mortality in septic patients. The sepsis-induced damage of
endothelial cell membrane gives rise to increased capillary permeability. Evidence suggests
that increased capillary permeability in patients with sepsis was associated with higher
incidence of MODS and death during the ICU stay than those with decreased permeability.
Angiopoietin (Ang) system is the key mediator for maintaining capillary permeability. Ang-2
triggers an inflammatory response and inducing permeability by activating the endothelium.
In contrast, Ang-1 is anti-inflammatory, can inhibit adhesion molecule expression and
attenuate permeability increase in different stimuli. The disrupted angiopoietin system has
been reported in patients with sepsis, but the association between angiotension and MODS in
septic patients has not been well addressed.
This study is designated to determine serum concentrations of Ang-1, Ang-2, Ang-1/Ang-2
ratio, and Tie-2 in patients with sepsis-induced MODS and to investigate the association
among increased permeability, inflammatory mediators,autonomic dysfunction, and these serum
mediators in development of organ failure. In addition, the study will incubate endothelial
cells with septic patients' serum or tumor necrosis factor (TNF)-alfa, and determine the
effects of ang-1 administration and blockade of ang-2 on disruption of endothelial cell
structure, permeability increase, and expression of adhesion molecules. The study will also
determine the signaling pathways and altered NF-kB dimmer composition that is responsible
for the inhibitory effect for ang-1 administration on TNF-alfa-induced intercellular
adhesion molecule (ICAM)-1 expression on endothelial surface.
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Observational Model: Cohort, Time Perspective: Prospective
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