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Objective To investigate the expression of CD14/CD16 by monocytes and the anti-inflammatory effects of hypertonic saline plus dextran (HSD) in adult blunt trauma patients in hemonhagic shock. Method A total of 30 adult patients were eligible for inclusion in the study if they sustained blunt trauma from March to October 2007 and had at least one recorded episode of hypotension (systolic blood pressure ≤ 90 mm Hg) with clear evidence of blood loss (external or internal including the thorax, abdomen or retroperitoneum). Patients were excluded if they refused to participate, were admitted ≥ 6 hours after injury, were pregnant, or had chronic disease. The enrolled patients were randomly divided in a double-blinded manner into an HSD group which was administered 7.5% Nad plus 6% dextran - 70, and a control group which was administered 0.9% NaCl. A single 250 ml dose of either HSD or NaO was immediately administered to the patients in each of the two groups while they were in the emergency room. The primary outcomes were to measure the changes in CD4/CD16 expression by monocytes and the levels of anti-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-lra and IL-10. Patient demographics, fluid requirements, organ dysfunction, infection and death were recorded. Results A total of 28 patients were enrolled with no significant differences in their clinical measurements. Hyperosmolarity was modest and transient. HSD altered the shock-induced monocyte redistribution pattern by reducing the drop in the "classic" CD14 ++ subset and remarkably affecting the expansion of the "pro-inflammatory" CD14+CD16+ subsets. In parallel, HSD significamly reduced pro-inflammatory TNF-α production while increasing anti-inflammatory IL-lra and IL-10 production. Conclusions This human trial demonstrates that HSD has anti-inflammatory and immunologic properties for trauma patients in hemorrhagic shock. HSD exerts profound immunomodulatory effects, promoting more balanced pro-/anti-inflammatory responses and reducing post-traumatic complications. Therefore, it could be useful in attenuating post-trauma multiorgan dysfunction (MOD).

8.Association between fibrinogen and carotid atheromatous plaque in patients with ischemic stroke

Wei CHEN ; Jie CHENG ; Genfa WANG ; Xinghua CHEN

Chinese Journal of Tissue Engineering Research 2006;10(46):212-213

BACKGROUND: Increase of fibrinogen is an independent risk factor for cardio-cerebrovascular disease and peripheral angiopathy. Fibrinogen and its degradation product exist in carotid atheromatous plaque and it can stimulate proliferation and migration of smooth muscle cells so as to play a key role in early atherosclerosis.OBJECTIVE: To analyze the relationship between plasma fibrinogen and carotid atheromatous plaque.DESIGN: Descriptive observation.SETTING: Department of Neurology, Xinhua Hospital, Medical Collegeof Shanghai Jiaotong University.PARTICIPANTS: A total of 81 patients with ischemic stroke were selected from Neurological Department of Xinhua Hospital affiliated to Medical College of Shanghai Jiaotong University from September to December 2001.There were 53 males and 28 females aged 41-85 years with the mean age of (65±11) years.METHODS: On the basis of carotid ultrasonography, 81 patients with ischemic stroke were divided into present plaque group (n=45) and absent plaque group (n=36) to measure plasma fibrinogen, serum total cholesterol (TC), low density lipoprotein cholesterol (LDL-C) and other risk factors of atherosclerosis so as to observe the correlation between risk indexes and carotid atheromatous plaque.MAIN OUTCOME MEASURES: Risk indexes of carotid atherosclerosis and carotid atheromatous plaque.RESULTS: All 81 patients were involved in the final analysis. ① Values of fibrinogen, TC and LDL-C in present plaque group were (4.38±1.33) g/L,(5.19±1.27) mmol/L and (3.15±0.37) mmol/L, respectively, which were higher than those in absent plaque group [(3.20±1.30) g/L, (4.56±1.30) mmol/L,(2.49±0.92) mmol/L, P ＜ 0.05]. ② Ratios of carotid atheromatous plaque were 11% (5 cases), 16% (7 cases) and 73% (33 cases) in fibrinogen groups at Iow, moderate and high dosages, respectively. There was significant difference (P =0.002). ③ Multiple factor analyses of carotid atherosclerosis showed that the risk factors which promoted the formation of carotid atheromatous plaque were diabetes mellitus, low density lipoprotein (LDL), fibrinogen and age growing.CONCLUSION: Fibrinogen plays an active role in development and progression of carotid atheromatous plaque.