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

Citation
T. Shimizu et al., The role of bacterial translocation on neutrophil activation during hemorrhagic shock in rats, SHOCK, 16(1), 2001, pp. 59-63
Citations number
35
Categorie Soggetti
Aneshtesia & Intensive Care","Cardiovascular & Hematology Research
Journal title
SHOCK
ISSN journal
10732322 → ACNP
Volume
16
Issue
1
Year of publication
2001
Pages
59 - 63
Database
ISI
SICI code
1073-2322(200107)16:1<59:TROBTO>2.0.ZU;2-M
Abstract
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.