HYPERTONIC SALINE RESUSCITATION DIMINISHES LUNG INJURY BY SUPPRESSINGNEUTROPHIL ACTIVATION AFTER HEMORRHAGIC-SHOCK

Citation
N. Angle et al., HYPERTONIC SALINE RESUSCITATION DIMINISHES LUNG INJURY BY SUPPRESSINGNEUTROPHIL ACTIVATION AFTER HEMORRHAGIC-SHOCK, Shock, 9(3), 1998, pp. 164-170
Citations number
33
Categorie Soggetti
Peripheal Vascular Diseas","Emergency Medicine & Critical Care",Hematology
Journal title
ShockACNP
ISSN journal
10732322
Volume
9
Issue
3
Year of publication
1998
Pages
164 - 170
Database
ISI
SICI code
1073-2322(1998)9:3<164:HSRDLI>2.0.ZU;2-U
Abstract
Hypertonic saline (HS) resuscitation after hemorrhage and sepsis has b een shown to markedly reduce the development of lung injury in animals , compared with traditional resuscitation with lactated Ringer's (LR). These experiments examined the effect of HS on lung injury after hemo rrhage without sepsis. The effects of HS and LR resuscitation on neutr ophil trafficking, neutrophil adhesion, and neutrophil oxidative burst were studied. Methods: BALB/c mice were hemorrhaged to a mean arteria l pressure of 40 torr for 1 h. Animals were resuscitated with shed blo od and either 4 mL/kg of 7.5% HS or LR in twice the volume of the shed blood. Lung histology was examined 24 h after hemorrhage. Lung myelop eroxidase content and bronchoalveolar lavage fluid neutrophil counts w ere obtained. Peripheral blood smears were obtained to determine the n eutrophil percentage. Peripheral blood neutrophil CD11b expression and neutrophil H2O2 production were assayed by flow cytometry. Results: H S animals had less lung injury than LR animals. The mean myeloperoxida se activity in HS versus LR animals was 1.79 +/- 1.33 U/100 mg versus 3.0 +/- 1.33 U/100 mg, respectively. The percentage of neutrophils in the bronchoalveolar ravage fluid of HS animals (3.8% +/- .8) was signi ficantly less than that of LR animals (10.8% +/- 2.1). This correspond ed to a significantly higher peripheral blood neutrophil count in HS a nimals compared with LR animals, 41% vs. 20%, respectively. There was no difference in neutrophil expression of the CD11b integrin between t he HS and LR groups. The neutrophils of LR animals had basal H2O2 prod uction that was 107% greater than that of controls; HS suppressed this hemorrhage-induced activation by > 60%. HS resuscitation after hemorr hagic shock protects against the development of lung injury. This prot ection is due, in part, to suppression of the hemorrhage-induced neutr ophil oxidative burst. HS resuscitation offers immunomodulatory potent ial after hemorrhagic shock.