HYPOTHESIS: Inhibition of neutrophil-endothelial cell interactions by hypertonic saline (HTS) may confer protection against organ injury in states of immunologic disarray. This study tested the hypothesis that infusion of HTS modulates the development of end-organ injury in a model of lower-torso ischemia-reperfusion injury. DESIGN: Ischemia-reperfusion injury was induced in 30 male Sprague-Dawley rats by infrarenal aortic cross-clamp for 30 minutes, followed by reperfusion for 2 hours. At 0 and 60 minutes of reperfusion, intravenous HTS (7.5% sodium chloride, 4 mL/kg) was administered to 6 rats each, and another 12 received either 4 or 30 mL/kg of isotonic sodium chloride solution. Six rats received HTS, 4 mL/kg, before ischemia. At 2 hours, we assessed liver function, pulmonary injury, neutrophil infiltration (myeloperoxidase activity), endothelial permeability (bronchoalveolar lavage and wet-dry weight ratios), and proinflammatory cytokine levels (tumor necrosis factor alpha and interleukin 6). RESULTS: Infusion with HTS before or after ischemia significantly reduced end-organ injury. Histopathologic pulmonary injury scores were markedly attenuated in the HTS group (5.82 +/- 1.3) and the HTS pretreated group (4.91 +/- 1.6) compared with the isotonic sodium chloride solution groups (8.54 +/- 1.1) (P =.04). Pulmonary neutrophil sequestration (2.07 +/- 0.23) and increased endothelial permeability (4.68 +/- 0.44) were manifest in animals resuscitated with isotonic sodium chloride solution compared with HTS treatment (1.54 +/- 0.19 [P =.04] and 2.06 +/- 0.26 [P =.02]) and pretreatment (1.18 +/- 0.12 [P =.04] and 1.25 +/- 0.07 [P =.002]). In addition, a significant reduction in serum tumor necrosis factor alpha (P =.04) and interleukin 6 (P =.048) levels was observed, whereas HTS resuscitation attenuated the upsurge in aspartate transaminase (P =.03) and alanine transaminase levels (P =.047). CONCLUSIONS: Resuscitation with HTS attenuates the pulmonary edema and tissue injury due to lower-torso ischemia-reperfusion and maintains a more benign immunologic profile.
HYPOTHESIS: Inhibition of neutrophil-endothelial cell interactions by hypertonic saline (HTS) may confer protection against organ injury in states of immunologic disarray. This study tested the hypothesis that infusion of HTS modulates the development of end-organ injury in a model of lower-torso ischemia-reperfusion injury. DESIGN:Ischemia-reperfusion injury was induced in 30 male Sprague-Dawley rats by infrarenal aortic cross-clamp for 30 minutes, followed by reperfusion for 2 hours. At 0 and 60 minutes of reperfusion, intravenous HTS (7.5% sodium chloride, 4 mL/kg) was administered to 6 rats each, and another 12 received either 4 or 30 mL/kg of isotonic sodium chloride solution. Six rats received HTS, 4 mL/kg, before ischemia. At 2 hours, we assessed liver function, pulmonary injury, neutrophil infiltration (myeloperoxidase activity), endothelial permeability (bronchoalveolar lavage and wet-dry weight ratios), and proinflammatory cytokine levels (tumor necrosis factor alpha and interleukin 6). RESULTS: Infusion with HTS before or after ischemia significantly reduced end-organ injury. Histopathologic pulmonary injury scores were markedly attenuated in the HTS group (5.82 +/- 1.3) and the HTS pretreated group (4.91 +/- 1.6) compared with the isotonic sodium chloride solution groups (8.54 +/- 1.1) (P =.04). Pulmonary neutrophil sequestration (2.07 +/- 0.23) and increased endothelial permeability (4.68 +/- 0.44) were manifest in animals resuscitated with isotonic sodium chloride solution compared with HTS treatment (1.54 +/- 0.19 [P =.04] and 2.06 +/- 0.26 [P =.02]) and pretreatment (1.18 +/- 0.12 [P =.04] and 1.25 +/- 0.07 [P =.002]). In addition, a significant reduction in serum tumor necrosis factor alpha (P =.04) and interleukin 6 (P =.048) levels was observed, whereas HTS resuscitation attenuated the upsurge in aspartate transaminase (P =.03) and alanine transaminase levels (P =.047). CONCLUSIONS: Resuscitation with HTS attenuates the pulmonary edema and tissue injury due to lower-torso ischemia-reperfusion and maintains a more benign immunologic profile.
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