Reduced rate of bacterial translocation and improved variables of natural killer cell and T-cell activity in rats surviving controlled hemorrhagic shock and treated with hypertonic saline

OBJECTIVE To examine the effect of hypertonic saline on bacterial translocation and the number and function of natural killer and T cells in controlled hemorrhagic shock. DESIGN Randomized controlled study. Duration of follow-up was 24 hrs. SETTING University research laboratory. SUBJECTS Adult male Sprague-Dawley rats, weighing 310–390 g. INTERVENTIONS Controlled hemorrhagic shock was induced by blood withdrawal (mean arterial pressure, 30–40 mm Hg) and maintained for 30 mins. The animals were randomly divided into three groupsgroup 1 (n = 10) was sham-operated, group 2 (n = 10) was untreated, and group 3 was treated with 5 mL/kg hypertonic saline (n = 10). The rats were killed after 24 hrs. MEASUREMENTS AND MAIN RESULTS Infusion of hypertonic saline in group 3 was followed by reduced bacterial translocation rate (5.0 ± 2.2% vs. 18.3 ± 5.3%, p < .033). The total mass of bacteria isolated from hypertonic saline-treated animals with bacterial translocation was 7.8- to 10.4-fold less than that from untreated rats. Controlled hemorrhagic shock resulted in a low percentage of CD4+ cells in blood (35.2 ± 3.9%, p < .05) and lymph nodes (44.4 ± 4.5%, p < .05) and depressed CD4 expression on blood (82 ± 13 arbitrary units, p < .005) and lymph node (168 ± 24 arbitrary units, p < .03) cells. A compensatory mobilization of NKR-P1+ cells from lymph nodes (8.6 ± 2.3%, p < .05) to blood (21.2 ± 5.2%, p < .01) with down-regulated NKR-P1 expression on blood cells (59 ± 10 arbitrary units, p < .005) was observed. Natural killer cell-mediated cytotoxicity was decreased (67.9 ± 9.7%, p < .05). Hypertonic saline treatment greatly stimulated CD4 expression on blood (419 ± 113 arbitrary units, p < .005) and lymph node (553 ± 115 arbitrary units, p < .03) cells. Also, normalization of NKR-P1 expression (160 ± 19 arbitrary units, p < .005) and restoration of natural killer cell-mediated cytotoxicity to near normal values (88.6 ± 7.4%, p < .05) were demonstrated. CONCLUSION Controlled hemorrhagic shock was accompanied by CD4+ cells suppression and excessive recruitment of natural killer cells with abnormally low NKR-P1 expression and suppressed cytolytic activity into circulation. Infusion of hypertonic saline reversed these changes and reduced bacterial translocation.