The role of bacterial translocation on neutrophil activation during hemorrhagic shock in rats.

Some biological responses to hemorrhage have been reported to be associated with bacterial translocation (BT). While the relationship between peripheral 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 and priming during hemorrhagic shock. The experimental rats were divided into three groups: a group with normal intestinal flora (NF group), an antibiotic-decontaminated group (AD group), and a sham shock group with normal intestinal 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 occurrence of BT. Hydrogen peroxide generation and CD11b/c expression were assayed by flow cytometry to evaluate peripheral blood neutrophil activation and priming, respectively. In the NF group, significant BT to the MLNs and spleen was noted from 30 min after the shock induction, and significant hydrogen peroxide generation was also noted from 30 min. The expression of CD11b/c on neutrophils was significantly up-regulated at 90 min after the shock induction. Furthermore, BT, as also the aforementioned parameters of neutrophil 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 influence the host responses starting from the early phase of damage, even in noninfectious stress-inducing conditions.