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KMID : 0371319960500050634
Journal of the Korean Surgical Society
1996 Volume.50 No. 5 p.634 ~ p.639
TNF Changes after Hemorrhagic Shock in Rats



Abstract
TNF (Tumor Necrosis Factor) is one of the polypeptide cytokines involving inflammatory reaction, immune system, and metabolism. This 17KD sized trimer molecule is known to act as a key mediator in septic shock and multiple organ failure. When the
substance is activated, interleukins are activated subsequently in cascade system and polymorphoneucleocytes, and microcirculation is also impaired. In hemorrhagic shock, microcirculatory derangement owing to the endothelial damage is suspected
as
one
of a possible pathophysiologic mechanisms. So, one could correlate the pathophysiology of hemorrhagic shock with the increase of the TNF easily. The aim of this study is to clarify the increase of TNF in hemorrhgic shock and to investigate the
relation
between the increase of TNF and mortality rate in the rats. Fifteen Sprague- Ddawley rats were used. Anesthesia was done with intraperitoneal ketamin injection. The left femoral artery was cannulated and connected to the pressure monitor. The
left
femoral vein was used as a route for bleeding, resuscitation and sampling. Bleeding was performed via the femoral vein to reach mean arterial pressure of 20~30mmHg for 60 minutes. Then the shed blood was returned with normal saline to reach
original
mean arerial pressure level. The animals were returned to their cages for observations for 48 hours. Sampling was done before shock, and 60 minutes after shock. The control animals were cannulated in the same manner and blood was sampled
immediately and
90 minutes later without producing shock. The samples were centrifuged and plasma was seaparated, and stored at -70¡É before use for TNF assays. TNF analysis was done with ELISA kit. The changes in TNF level was determined by the ratio of TNF
level
after shock to the level before shock. The ratio was 2.19 (¡¾1.03) in the shock group and 1.12(¡¾0.38) in the control group. After 48 hours, 50% (4/8) of rats died in the shock group. On the contrary, there was no mortality in the control group.
As
a
conclusion, authors found that TNF increases in hemorrhagic shock and it might be related with the high mortality in hemorrhagic shock. Further study should investigate the mechanism of this phenomenon.
KEYWORD
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