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

Abstract

Background: Hypertonic saline (HTS) has been noted previously to reduce neutrophil activation. The aim of this study was to elucidate the effect of hypertonic resuscitation on the development of end-organ damage in an animal model of pancreatitis.Methods: Pancreatitis was induced in Sprague–Dawley rats by intraperitoneal injection of 20 per cent l-arginine. Animals were randomized into four groups (each n = 8): controls; pancreatitis without intervention; pancreatitis plus intravenous resuscitation with normal saline (0·9 per cent sodium chloride 2 ml/kg) at 24 and 48 h; or HTS (7·5 per cent sodium chloride 2 ml/kg) at these time points. Pulmonary endothelial leakage was assessed by measurement of lung wet: dry ratios, bronchoalveolar lavage protein and myeloperoxidase 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 scores 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 protein content 1287 μg/ml) were evident in animals resuscitated with normal saline compared with HTS (1·22 units/g and 277 μg/ml respectively; P < 0·02).Conclusion: HTS resuscitation results in a significant attenuation of end-organ injury following a systemic inflammatory response to severe pancreatitis.