Hypertonic Saline reduces inflammation and enhances the resolution of Oleic Acid induced Acute Lung Injury.


Hypertonic saline (HTS) reduces the severity of lung injury in ischemia-reperfusion, endotoxin-induced and ventilation-induced lung injury. However, the potential for HTS to modulate the resolution of lung injury is not known.

We investigated the potential for hypertonic saline to modulate the evolution and resolution of oleic acid induced lung injury.

Methods: Adult male Sprague Dawley rats were used in all experiments.

Series 1 examined the potential for HTS to reduce the severity of evolving oleic acid (OA) induced acute lung injury. Following intravenous oleic acid administration, animals were randomized to receive 4ml/Kg of isotonic (0.9% saline, Control, n=12) or hypertonic saline (7.5% saline, HTS, n=12), and the lung injury was assessed at 4 hours.

Series 2 examined the potential for HTS to enhance the resolution of oleic acid (OA) induced acute lung injury. Following intravenous OA administration, animals were randomized to receive isotonic (Control, n=6) or hypertonic saline (HTS, n=6), and the extent of lung injury was assessed after 6 hours.

Results: In Series I, HTS significantly reduced bronchoalveolar lavage (BAL) neutrophil counts compared to Control [24.5 +/- 5.69 versus 44.0 +/- 4.75 x10^3 cells/ml]. However, there were no between group differences with regard to: Alveolar-arterial oxygen gradient [10.8 +/- 0.5 versus 11.0 +/- 0.7 KPa]; arterial oxygen tension; static lung compliance, or histologic injury.

In contrast, in Series 2, hypertonic saline significantly reduced histologic injury and reduced BAL neutrophil counts [61.5 +/- 9.1 versus 102.6 +/- 11.9 x10^3 cells/ml], and interleukin-6 levels [1540 +/- 287 vs. 2046 +/- 309 pg/ml]

Conclusions: These findings demonstrate, for the first time, the potential for HTS to reduce pulmonary inflammation and enhance the resolution of oleic acid induced lung injury.



Author: Muiris T Kennedy, Brendan D Higgins, Joseph F Costello, William A Curtin and John G Laffey
Credits/Source: BMC Pulmonary Medicine 2008, 8:9



Published on: 2008-07-08

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