The present study was designed to investigate the production of tumor necrosis factor a （TNFα） in-duced by low-dose （1μg/kg） lipopolysaccharide （LPS） and its cellular source after hemorrhagic shock（HS） in rats

and to further analyze the mechanism for increased sensitivity to LPS through looking at ex-pression of lipopolysaccharide -binding protein （LBP ） mRN A in t he liver

lungs and kidneys. lt wa s foundin uiuo that plasma TNFa levels in the HS+LPS group were 20-fold higher than that in the HS group （P<0. 01 ）

and 2. 7-fold higher than that in the LPS group （P<0. 05）. lt was shown in ndro that the ca-pacity of peripheral white blood cells to produce TNFa in response to LPS stimulation was significantly de-creased by 126 % （P<0. 01 ） and 57% （P<0. 05） compared with pre-shock levels and the sham group re-spectively at the end of resuscitation following shock

and was still markedly decreased 3 hours after resus-citation

while the capacity of Kupffer Cells was significantly increased by 110% compared with the shamgroup （P<0. 01） after shock and resuscitation. Results from RT-PCR showed that expression of LBPmRNA in the liver

lungs and kidneys was increased after shock and resuscitation. It is suggested thathemorrhagic shock could significantly enhance endotoxin-induced TNFa production

which might be due toup-regulation of LBP expression in tissues after shock

and tissue macrophages might be the main source ofcytokine production.