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Updated: Aug 10, 2026
Endotoxin Activity Assay for the Detection of Whole Blood Endotoxemia in Critically Ill Patients
Published on: June 24, 2019
[Influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic
Yong-jun Wei1, Rui-lan Wang, Guo-ping Li
1Emergency Department, The Second Affiliated Hospital of Jiangxi Medical College, Nanchang 330006, Jiangxi, China.
Objective:
To investigate the influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats.
Methods:
Eighty male SD rats were randomly divided into two groups: control and cobra venom factor (CVF) treatment groups. The hemorrhagic shock induced by trauma was replicated in both groups. The animals were killed preshock and at 1, 6, and 24 hours postresuscitation. Twenty-four hours before hemorrhage, rats were given a mainline dose of either 50 microg/kg CVF or an equal volume of saline solution. The plasma and serum samples were collected at each time point to determine the concentration of endotoxin, the activity of CH50 and diamine oxidase (DAO), and the level of tumor necrosis factor (TNF-alpha) at various time points in two groups.
Results:
Compared with preshock in control group, serum CH50 levels were decreased promptly at 1 hour postresuscitation. Markedly elevation of the levels of endotoxin and TNF-alpha in blood were found at early time after resuscitation, and they were come rapidly back to the basic level at 6 and 24 hours phase. The activity of DAO in blood was increased significantly at 1 and 6 hours after resuscitation and declined promptly at 24 hours. Compared with the control group, significantly decline of the levels of endotoxin, TNF-alpha and DAO at the various time points after resuscitation were also found in the CVF group. The levels of CH50 in CVF group were always less than 5% during the experiment.
Conclusion:
In traumatic hemorrhagic shock rats CVF pretreatment could decline plasma endotoxin levels by preventing the injury of intestine and gut barrier function, decrease endotoxin translocation and reduce plasma endotoxin levels.
