Sympathetic excitation and dendritic cell activation aggravates myocardial injury in LPS-induced rats / 基础医学与临床

Objective To investigate the effects of sympathetic excitation and dendritic cell activation on myocar-dial injury in LPS-induced rats. Methods The rats were randomly divided into four groups:control group, LPS group ( intraperitoneal injection of LPS 10 mg/kg) ,intervention group ( given beta receptor blocker Ate 5 mg/kg after LPS administration) and DC inhibitor VAG539 intervention group ( VAG539 30 mg/kg gavage twice a day for 2 days after LPS administration) respectively . The powerlab system was used to record the hemodynamic and sympathetic data. The concentration of norepinephrine ( NE) in plasma was measured by high performance liquid chromatography ( HPLC) , and the expression and positive cells of TNF-α and DCs in myocardium were detected by immunohistochemistry. Results Compared with the control group, the plasma NE level significantly increased ( P＜0.05) ;The expression of TNF-α and DCs in heart tissue significantly increased ( P＜0.05) ;the renal sym-pathetic nerve activity (SNA) significantly increased in the three groups after LPS administration for 24 hours. Compared with the LPS group, the plasma NE level significantly decreased ( P＜0.05 ) ; The expression of TNF-α and DCs in heart tissue significantly decreased ( P＜0.05) ;the renal SNA significantly decreased after Ate and VAG539 administration(P＜0.05).Conclusions Excessive activation of sympathetic nervous system and activation of DC aggravate myocardial injury in LPS-induced rats.

Application of simulation training for central venous catherteriazation in emergency department / 基础医学与临床

Objective To compare the simulaion training with traditional training on central venous cathertrization(CVC). Methods Forty emergency residents from a teaching hospital were selected from May 2016 to May2017, and they were randomly assigned into two groups: simulation group (SG) and traditional group(TG). After the training they must completed one CVC and filled in a questionaire. The success rate, puncture time, trail time and complication rate between the two groups were compared. Results There were 18 students on tradional group(TG) and 19 students on simulation group(SG) who completed the whole procedure(complete the procedure in-dependently and filled in the questionaire). The success rate of SG and TG were 73.7％ and 33.3％ respectively (P＜0.05).the lengthen of procedure was (21.3±4.0) min on SG and (31.3±5.9) min on TG, The trail times were (2.1±1.0) on SG and (4.5±1.0) on TG, the complication rate was 16％±37％ on SG and 38％±50％ on TG, compared with TG, the lengthen of procedure on SG was significantly shortened (P＜0.05), the trail times on SG were significantly reduced (P < 0.05) and the complication rate significantly decreased (P <0.05). Conclusions The simulation training significantly improved the success rate of CVC, shortened the lengthen of procedure, decreased the trail times and complication rate. It deserved teaching hospitals to popularize-ing on standardized training for resident physicians.

Neutrophil Dysfunction in Sepsis / 中华医学杂志(英文版)

<p><b>OBJECTIVE</b>Sepsis is defined as life-threatening organ dysfunction due to a dysregulated host response to infection. In this article, we reviewed the correlation between neutrophil dysfunction and sepsis.</p><p><b>DATA SOURCES</b>Articles published up to May 31, 2016, were selected from the PubMed databases, with the keywords of "neutrophil function", "neutrophil dysfunction", and "sepsis".</p><p><b>STUDY SELECTION</b>Articles were obtained and reviewed to analyze the neutrophil function in infection and neutrophil dysfunction in sepsis.</p><p><b>RESULTS</b>We emphasized the diagnosis of sepsis and its limitations. Pathophysiological mechanisms involve a generalized circulatory, immune, coagulopathic, and/or neuroendocrine response to infection. Many studies focused on neutrophil burst or cytokines. Complement activation, impairment of neutrophil migration, and endothelial lesions are involved in this progress. Alterations of cytokines, chemokines, and other mediators contribute to neutrophil dysfunction in sepsis.</p><p><b>CONCLUSIONS</b>Sepsis represents a severe derangement of the immune response to infection, resulting in neutrophil dysfunction. Neutrophil dysfunction promotes sepsis and even leads to organ failure. Mechanism studies, clinical practice, and strategies to interrupt dysregulated neutrophil function in sepsis are desperately needed.</p>