Some biological responses to hemorrhage have been reported to be associated
with bacterial translocation (BT), While the relationship between peripher
al blood neutrophils and BT in the late phase of hemorrhagic shock or burn
injury has been reported, this relationship in the early phase has not been
fully elucidated. We investigate the role of BT in neutrophil activation a
nd priming during hemorrhagic shock. The experimental rats were divided int
o three groups: a group with normal intestinal flora (NF group), an antibio
tic-decontaminated group (AD group), and a sham shock group with normal int
estinal flora (sham group). Hemorrhagic shock was induced in the NF and AD
groups (MAP 30 mm Hg for 30-90 min). The rats were sacrificed at 30, 60, or
90 min following the shock induction. Cultures were taken from the liver,
spleen, mesenteric lymph nodes (MLNs), and systemic blood to assess the occ
urrence of BT. Hydrogen peroxide generation and CD11b/c expression were ass
ayed by flow cytometry to evaluate peripheral blood neutrophil activation a
nd priming, respectively. In the NF group, significant BT to the MLNs and s
pleen was noted from 30 min after the shock induction, and significant hydr
ogen peroxide generation was also noted from 30 min. The expression of CD11
b/c on neutrophils was significantly up-regulated at 90 min after the shock
induction. Furthermore, BT, as also the aforementioned parameters of neutr
ophil function, was significantly suppressed in the AD group. We, therefore
, concluded that neutrophil activation and priming during hemorrhagic shock
might be closely related to BT, and that infectious factors possibly influ
ence the host responses starting from the early phase of damage, even in no
ninfectious stress-inducing conditions.