Abstract | BACKGROUND:
Granulocyte colony-stimulating factor ( G-CSF) increases production and release of neutrophil precursors and activates multiple functions of circulating polymorphonuclear neutrophils (PMNs). G-CSF has therapeutic effects in many experimental models of sepsis; its actions with superimposed reperfusion insults are unknown. In traumatic conditions, G-CSF could exacerbate unregulated, PMN-dependent injury to otherwise normal host tissue or, it could partially reverse trauma-induced immune suppression, which may improve long-term outcome. This study tested whether stimulating PMN proliferation and function with G-CSF during recovery from trauma+sepsis potentiated reperfusion injury or whether it improved host defense. METHODS: RESULTS: Neutrophilia and localization of infection, were significantly improved by G-CSF. Variables altered by G-CSF, though not significantly, showed GO2B potential increased by 50%, lipopolysaccharide- tumor necrosis factor decreased by 50%, and improved survival versus placebo (100% vs. 70%). G-CSF did not increase lung MPO, BAL cell count, or BAL protein. Both arterial and venous O2 saturations were unaltered. CONCLUSIONS:
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Authors | J H Patton Jr, S P Lyden, D N Ragsdale, M A Croce, T C Fabian, K G Proctor |
Journal | The Journal of trauma
(J Trauma)
Vol. 44
Issue 5
Pg. 750-8; discussion 758-9
(May 1998)
ISSN: 0022-5282 [Print] United States |
PMID | 9603074
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, Non-P.H.S.)
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Chemical References |
- Granulocyte Colony-Stimulating Factor
- Oxygen
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Topics |
- Animals
- Disease Models, Animal
- Female
- Granulocyte Colony-Stimulating Factor
(therapeutic use)
- Leukocyte Count
- Lung
(immunology, pathology)
- Male
- Neutrophils
(cytology, drug effects, physiology)
- Oxygen
(blood)
- Reperfusion Injury
(prevention & control)
- Resuscitation
- Sepsis
(drug therapy, immunology, microbiology)
- Shock, Hemorrhagic
(drug therapy, immunology)
- Swine
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