Hypertonic saline attenuates end-organ damage in an experimental model of acute pancreatitis

Background: Hypertonic saline (HTS) has been noted previously to reduce neu trophil activation. The aim of this study was to elucidate the effect of hy pertonic resuscitation on the development of endorgan damage in an animal m odel of pancreatitis. Methods: Pancreatitis was induced in Sprague-Dawley rats by intraperitoneal injection of 20 per cent L-arginine. Animals were randomized into four gro ups teach n=8): controls; pancreatitis without intervention; pancreatitis p lus intravenous resuscitation with normal saline (0.9 per cent sodium chlor ide 2ml/kg) at 24 and 48h; or HTS (7.5 per cent sodium chloride 2ml/kg) at these time points. Pulmonary endothelial leakage was assessed by measuremen t of lung wet:dry ratios, bronchoalveolar lavage protein and myeloperoxidas e activity. Results: Animals that received HTS showed less pancreatic damage than those resuscitated with normal saline (1.0 versus 3.0; P = 0.04). Lung injury sc ores were also significantly diminished in the HTS group (1.0 versus 3.5; P = 0.03). Pulmonary neutrophil sequestration (myeloperoxidase activity 1.80 units/g) and increased endothelial permeability (bronchoalveolar lavage pr otein content 1287 mu g/ml) were evident in animals resuscitated with norma l saline compared with HTS (1.22units/g and 277 mu g/ml respectively; P < 0 .02). Conclusion: HTS resuscitation results in a significant attenuation of end-o rgan injury following a systemic inflammatory response to severe pancreatit is.