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 ...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 30e35 mmHg for 90 min followed by resuscitation over 50 min） were challenged with Lipopolysaccharide （LPS）, 1 mg/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 C. 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-a in HSR-LPS and HSR-LPS24 groups （1835 ± 478, 273 ± 77, 498 ± 200 pg/mL, respectively）. Compared to CON the LPS-induced TNF-a 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.展开更多
文摘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 30e35 mmHg for 90 min followed by resuscitation over 50 min） were challenged with Lipopolysaccharide （LPS）, 1 mg/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 C. 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-a in HSR-LPS and HSR-LPS24 groups （1835 ± 478, 273 ± 77, 498 ± 200 pg/mL, respectively）. Compared to CON the LPS-induced TNF-a 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.
