Hypertonic saline attenuation of the neutrophil cytotoxic response is reversed upon restoration of normotonicity and reestablished by repeated hypertonic challenge

Surgery
D J CieslaC C Silliman

Abstract

Hypertonic saline (HTS) resuscitation, in addition to enhancing hemodynamic recovery, modulates postinjury hyperinflammation in the critically injured. The polymorphonuclear neutrophil (PMN) cytotoxic response, a key element in the pathogenesis of postinjury organ dysfunction, is attenuated under hypertonic conditions. Although plasma Na(+) rises to 180 mmol/L after HTS infusion, baseline levels are reestablished within 24 hours. We hypothesized that HTS attenuation of the PMN cytotoxic response (beta2-integrin expression, elastase release, and O2- production) is reversed upon return to normotonicity, but can be reestablished by repeated HTS challenge. Isolated human PMNs were incubated in HTS (Na(+) = 180 mmol/L) for 5 minutes at 37 degrees C then returned to normotonicity by centrifugation and resuspension in isotonic buffer. Stimulated (PAF) beta2-integrin expression was measured by flow cytometry. Stimulated (PAF/fMLP) elastase release and O2- production were measured by cleavage of N-methoxysuccinyl-Ala-Ala-Pro-Val p-nitroanilide and reduction of cytochrome c (Cyt c). Protein tyrosine phosphorylation in PMN cell lysates was assessed by Western blot. Clinically relevant levels of HTS induced tyrosine phosphorylation in rest...Continue Reading

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Citations

Jun 19, 2007·Neurosurgical Review·R TyagiJ Jallo
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