• Issue 5,2008 Table of Contents
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    • Treatment of sepsis

      2008, 7(5):293-296.

      Abstract (26) HTML (0) PDF 944.00 Byte (81) Comment (0) Favorites

      Abstract:

      全身性损伤因素包括感染和非感染性因素(如感染、休克、创伤、重症胰腺炎等)可导致全身性炎症反应综合征(SIRS),在此基础上发生感染可诱发脓毒症(sepsis),进而发展成严重脓毒症(severe sepsis)和脓毒性休克(septic shock)。脓毒症也是多器官功能障碍综合征(MODS)的主要原因之一[1-2]。从1992年美国胸科学会(ACCP)和重症医学会(SCCM)联袂初步确立的SIRS的初步诊断标准[3]至2001年华盛顿会议重新制定脓毒症的概念[4]、2002年拯救脓毒症运动和巴塞罗那宣言、2004年由SCCM/欧洲危重病医学会(ESICM)/ACCP/美国胸科学会(ATS)/外科感染学会(SIS)发布的治疗指南[5],虽然大量研究对脓毒症的发病机制和临床治疗进行了深入探讨,但至今为止,还有许多问题没有得到根本解决。如脓毒症的定义和治疗标准尚未得到统一;病死率居高不下,甚至呈逐年上升趋势[6],包括活化蛋白C和控制血糖在内的30多项大型临床治疗方案均宣告失败[7];特别是脓毒症合并MODS所致的高病死率,使许多学者有意或无意地避开相关方面研究,导致脓毒症合并MODS的研究进展有所停滞。尽管如此,这些曲折的经历给脓毒症下一步的研究和临床治疗仍提供了宝贵经验。

    • Development of the model about concanavalin Ainduced experimental liver injury in mice

      2008, 7(5):397-301.

      Abstract (29) HTML (0) PDF 1.80 K (64) Comment (0) Favorites

      Abstract:

      ObjectiveTo establish the model about concanavalin Ainduced(Con A)experimental liver injury in mice. MethodsForty Balb/C mice were randomly divided into 4 groups(ten for each group), A, B, C and D. Con A 10mg/kg, 20mg/kg or 30mg/kg was intravenously (tail vein) injected into the mice in group A, B and C respectively while normal saline was used for the group D (control group). Activity of alanine transaminase(ALT), death rate  and liver histopathological changes were observed after 8 hours of injection. The optimal Con A dose (20mg/kg) was selected, activity of ALT, death rate  and liver histopathological changes were observed based on such dosage. ResultsAfter 8 hours of injection of Con A, no dead mouse was found in group A and D, but 3 and 10 mice were dead in group B and C respectively; the ALT level in group A and B was (215.55±70.19) IU /L and  (2 516.14±764.69) IU / L respectively, both were significantly higher than (57.30±12.21) IU /L in group D (t=-8.466, t=-10.143, respectively; both P=0.000). Liver  histopathology showed only degeneration of liver cells was present in group A, while degeneration, necrosis and liver inflammatory cells infiltration in group B and C. Within 24 hours of injection of 20mg/kg of Con A, the death rate, activity of ALT, liver inflammatory cells infiltration, hepatocyte degeneration and  necrosis  exacerbated with the prolongation of time. ConclusionThe optimal dosage to establish Con Ainduced experimental liver injury in mice is 20mg/kg, with the optimal observation time at 8 hours after intravenous (tail vein) injected.

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