Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Comparative Study
Influence of hypertonic saline on bacterial translocation in controlled hemorrhagic shock.
Translocation of enteric bacteria has been described in rats following hemorrhagic shock (HS). The aim of the present study was to evaluate the effect of hypertonic saline (HTS) on bacterial translocation (BT) in the setting of controlled HS in rats. The study included 2 arms. ⋯ We concluded that whereas assessed qualitatively, in this model of severe HS in rats, the hemorrhagic insult itself resulted in BT in most animals and treatment with NS, HTS, and blood resulted in reduced early mortality but did not alter significantly the translocation rate. Only the combination of HTS and blood resulted in reduced BT to distant sites. However, quantitative assessment showed that HTS significantly reduced the number of translocating bacteria.
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Comparative Study
The effect of trauma on neutrophil L-selectin expression and sL-selectin serum levels.
Among identified adhesion molecules, the L-selectin on neutrophils enables the first step of leukocyte adherence to activated endothelial cells. To allow firm adhesion of neutrophils, L-selectin is then split off the cell membrane. It was hypothetized that an increase of the constitutively high serum level of soluble L-selectin may indicate an ongoing pathological neutrophil sequestration to the endothelial cells associated with activation and injury of the cells. ⋯ The in vitro studies revealed evidence for binding of sL-selectin to endothelial cells independently on the presence of neutrophils. According to our data, increasing severity of the post-operative/posttraumatic course is associated with decreasing sL-selectin serum levels and also reduced neutrophil L-selectin expression. In view of the in vitro results, this probably indicates competitive enhanced binding of sL-selectin to endothelial cells, thus masking the elevated activation of neutrophils and their ability for endothelial adherence.