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Hypertonic saline attenuates end-organ damage in an experimental model of acute pancreatitis
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 ra...
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Published in: | British journal of surgery 2000-10, Vol.87 (10), p.1336-1340 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that cite this one |
Online Access: | Get full text |
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Summary: | 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. © 2000 British Journal of Surgery Society Ltd |
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ISSN: | 0007-1323 1365-2168 |
DOI: | 10.1046/j.1365-2168.2000.01626.x |