The effects of TNF-α and anti-TNF-αMcAb in myocardial injury of rats with traumatic hemorrhagic shock

Objective: To study the effects of Tumor Necrosis Factor-α (TNF-α) and anti-TNF-α Monoclonal Antibody (McAb) in myocardial injury of rats with traumatic hemorrhagic shock. Methods: Twenty-four adult male Sprague-Dawley (SD) rats were randomly divided into the control group (A1 group), lactate Ringer's solution resuscitation group (A2 group) and anti-TNF-αMcAb resuscitation group (A3 group). A knife was used to cut about 5 cm in the middle of abdomen in rats of the A2 and A3 groups. Animal models of traumatic hemorrhagic shock were established through the femoral artery bleeding. The A2 group was treated with lactate Ringer's solution resuscitation, A3 group was treated with lactate Ringer's solution resuscitation containing anti-tumor necrosis factor-α monoclonal antibody (3 mg•kg-1), while the A1 group was under the same conditions without blood loss and trauma. The contents of Superoxide Dismutase (SOD) and Malondialdehyde (MDA) in myocardium were measured. The levels of serum TNF-α and CK-MB were detected in every group. The pathological changes of myocardium were observed by light microscopy. Results: The levels of serum TNF-α, CK-MB and the content of MDA in myocardium were increased in A2 and A3 groups comparing with A1 group (P<0.05), while the content of SOD was decreased (P<0.05). The levels of TNF-α (106.85 ± 14.65 pg/ml), CK-MB (535.3 ± 96.7 U/L) and the content of MDA (4.403 ± 0.979 nmol/mgprot) in myocardium in A3 group were much lower than those in the A2 group (P<0.05), but the content of SOD (36.125 ± 2.558 U/mgprot) was increased compared with the A2 group (SOD 28.200 ± 3.752 U/mgprot) (P<0.05). The changes of myocardium histopathology were minor in the A3 group while the A1 group had no manifest change. Conclusions: TNF-α is an important media in myocardial injury induced by traumatic hemorrhagic shock. Anti-tumor necrosis factor-α monoclonal antibody can reduce myocardial injury, the mechanism perhaps antagonistic activity of TNF-α.