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
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.