[Influence on the concentration of plasma endotoxin by inhibition of complement activation in traumatic hemorrhagic shock rats].
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.


CONCLUSIONS
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.
Wei
Yong-jun
YJ
Emergency Department, The Second Affiliated Hospital of Jiangxi Medical College, Nanchang 330006, Jiangxi, China.
Wang
Rui-lan
RL
Li
Guo-ping
GP
D000818:Animals; D003167:Complement Activation / Q000187:drug effects*; D051056:Complement Inactivating Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D004546:Elapid Venoms / Q000494:pharmacology*; D004731:Endotoxins / Q000097:blood*; D008297:Male; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D012771:Shock, Hemorrhagic / Q000097:blood* / Q000276:immunology; D012774:Shock, Traumatic / Q000097:blood / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D051056:Complement Inactivating Agents; D004546:Elapid Venoms; D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha; C016310:cobra venom factor