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Hypertonic saline activates lipid-primed human neutrophils for enhanced elastase release
D A Partrick1, E E Moore, P J Offner
1Department of Surgery, Denver Health Medical Center, Colorado 80204, USA.
The Journal of Trauma
|April 29, 1998
Summary
Hypertonic saline (HTS) at high concentrations activates primed neutrophils, increasing elastase release. This finding suggests HTS may contribute to multiple organ failure during early postinjury resuscitation.
Area of Science:
- Immunology
- Critical Care Medicine
- Biochemistry
Background:
- Hypertonic saline (HTS) is being re-evaluated for postinjury resuscitation, with studies reaching serum Na+ concentrations of 170 mmol/L.
- While HTS affects T-cells and monocytes, its impact on neutrophils (PMNs) is less understood.
- Lipid mediators like platelet-activating factor (PAF) and leukotriene B4 (LTB4) prime PMNs for cytotoxicity, potentially contributing to multiple organ failure.
Purpose of the Study:
- To investigate the effect of HTS on polymorphonuclear neutrophil (PMN) superoxide (O2-) and elastase release.
- To determine if HTS stimulates PMNs primed by PAF and LTB4.
Main Methods:
- Human PMNs were primed with PAF or LTB4.
- Cells were exposed to varying Na+ concentrations (130-170 mmol/L) simulating HTS.
- Superoxide generation and elastase release were measured.
Main Results:
- HTS up to 170 mmol/L did not affect O2- or elastase release from quiescent PMNs.
- However, Na+ concentrations of 160 and 170 mmol/L significantly enhanced elastase release from PAF- and LTB4-primed PMNs.
- No significant effect on O2- production was observed in primed PMNs.
Conclusions:
- Clinically relevant concentrations of HTS activate lipid-primed neutrophils, enhancing elastase degranulation.
- Early postinjury resuscitation with HTS may promote multiple organ failure by activating PMN elastase release.
- These findings highlight a potential mechanism linking HTS administration to adverse outcomes in critically ill patients.