Purpose:It has been suggested that patients with traumatic insults are resuscitated into a state of an early systemic inflammatory response.We aimed to evaluate the influence of hemorrhagic shock and resuscitation (HSR) upon the inflammatory response capacity assessed by overall TNF-α secretion capacity of the host compared to its release from circulating leukocytes in peripheral circulation.Methods:Rats (8/group) subjected to HS (MAP of 30-35 mmHg for 90 min followed by resuscitation over 50 min) were challenged with Lipopolysaccharide (LPS),1 μg/kg intravenously at the end of resuscitation (HSR-LPS group) or 24 h later (HSR-LPS24 group).Control animals were injected with LPS without bleeding (LPS group).Plasma TNF-α was measured at 90 min after the LPS challenge.In addition,whole blood (WB) was obtained either from healthy controls (CON) immediately after resuscitation (HSR),or at 24 h post-shock (HSR 24).WB was incubated with LPS (100 ng/mL) for 2 h at 37 ℃.TNF-α concentration and LPS binding capacity (LBC) was determined.Results:Compared to LPS group,HSR followed by LPS challenge resulted in suppression of plasma TNF-α in HSR-LPS and HSR-LPS24 groups (1835 ± 478,273 ± 77,498 ± 200 pg/mL, respectively).Compared to CON the LPS-induced TNF-αt release capacity of circulating leukocytes ex vivo was strongly declined both at the end of resuscitation (HSR) and 24 h later (HSR24) (1012 ± 259,313 ± 154,177 ± 63 ng TNF/mL,respectively).The LBC in WB was similar between CON and HSR and only moderately enhanced in HSR24 (57 ± 6,56 ± 6,71 ± 5 ％,respectively).Conclusion:Our data suggest that the overall inflammatory response capacity is decreased immediately after HSR,persisting up to 24 h,and is independent of LBC.