HYPERTONIC SALINE RESUSCITATION RESTORES HEMORRHAGE-INDUCED IMMUNOSUPPRESSION BY DECREASING PROSTAGLANDIN E(2) AND INTERLEUKIN-4 PRODUCTION

It was previously shown that hypertonic saline (HTS) enhances in vivo and in vitro cellular immune function of normal mice and reverses in v itro prostaglandin E(2) (PGE(2))-induced immunosuppression of normal p eripheral blood mononuclear cells. Hemorrhage induces immunosuppressio n despite adequate isotonic fluid resuscitation. The effects of HTS re suscitation on immunosuppression following hemorrhage were studied. A mouse model of hemorrhagic shock was used. Bleeding was performed thro ugh a catheter placed in the femoral artery, Phytohemagglutinin-induce d splenocyte proliferation and interleukin (IL)-1, IL-2, IL-4, IL-6, I L-10, transforming growth factor beta, and PGE(2) plasma levels were m easured 2 and 24 hr following hemorrhage and resuscitation with lactat ed Ringer's and HTS. In vivo cellular immune function was measured usi ng a contact hypersensitivity test. Suppression of splenocyte prolifer ation (40%) 24 hr following hemorrhage occurred after lactated Ringer' s resuscitation. HTS prevented immunosuppression. In vivo cell-mediate d immune function 24 hr after hemorrhage was improved by HTS. HTS-resu scitated animals showed significantly lower levels of IL-4 and PGE(2), and slightly elevated levels of proinflammatory cytokines (IL-1, IL-2 , and IL-6). HTS reverses hemorrhage-induced T-cell suppression by red ucing the production and/or release of IL-4 and PGE(2). (C) 1996 Acade mic Press, Inc.