BACKGROUND: Hypertonic saline (HTS) has been proposed as a resuscitation strategy following trauma based on its ability to prevent organ dysfunction by exerting immunosuppressive effects on inflammatory cells, including neutrophils. Because these cells are central to the innate response to bacteria, we hypothesized that hypertonic treatment for hemorrhagic shock might alter the host response to bacterial contamination of the peritoneal cavity and therefore render the host more susceptible to invasive infection. METHODS: Male Sprague-Dawley rats were subjected to hemorrhagic shock and resuscitated with either lactated Ringer solution (RL) or HTS. After intraperitoneal injection of feces, Escherichia coli, or lipopolysaccharide, peritoneal neutrophil accumulation and bacterial clearance were studied. In some studies, lipopolysaccharide as an inflammatory stimulus was injected into both the peritoneal cavity and the lungs. RESULTS: Peritoneal neutrophil accumulation in response to each of the stimuli did not differ between RL- and HTS-resuscitated animals. Whereas emigration into the peritoneum activated neutrophils, there was no difference between resuscitation strategies, consistent with the finding that bacterial clearance did not differ between groups. Although peritoneal neutrophil sequestration was unaffected by resuscitation type, HTS still was able to prevent lung neutrophil accumulation compared to RL treatment. CONCLUSIONS: HTS resuscitation did not impair the host response to bacterial contamination of the peritoneal cavity. However, the ability of HTS to prevent lung neutrophil accumulation in this setting persisted. These findings suggest that peritoneal bacterial contamination should not be considered a contraindication to the use of HTS in the trauma setting associated with hemorrhagic shock.
BACKGROUND:Hypertonic saline (HTS) has been proposed as a resuscitation strategy following trauma based on its ability to prevent organ dysfunction by exerting immunosuppressive effects on inflammatory cells, including neutrophils. Because these cells are central to the innate response to bacteria, we hypothesized that hypertonic treatment for hemorrhagic shock might alter the host response to bacterial contamination of the peritoneal cavity and therefore render the host more susceptible to invasive infection. METHODS: Male Sprague-Dawley rats were subjected to hemorrhagic shock and resuscitated with either lactated Ringer solution (RL) or HTS. After intraperitoneal injection of feces, Escherichia coli, or lipopolysaccharide, peritoneal neutrophil accumulation and bacterial clearance were studied. In some studies, lipopolysaccharide as an inflammatory stimulus was injected into both the peritoneal cavity and the lungs. RESULTS: Peritoneal neutrophil accumulation in response to each of the stimuli did not differ between RL- and HTS-resuscitated animals. Whereas emigration into the peritoneum activated neutrophils, there was no difference between resuscitation strategies, consistent with the finding that bacterial clearance did not differ between groups. Although peritoneal neutrophil sequestration was unaffected by resuscitation type, HTS still was able to prevent lung neutrophil accumulation compared to RL treatment. CONCLUSIONS: HTS resuscitation did not impair the host response to bacterial contamination of the peritoneal cavity. However, the ability of HTS to prevent lung neutrophil accumulation in this setting persisted. These findings suggest that peritoneal bacterial contamination should not be considered a contraindication to the use of HTS in the trauma setting associated with hemorrhagic shock.