Objective To investigate the distribution and antibiotic resistance of clinical pathogen isolated from patients of intra-abdominal infection associated sepsis in surgical intensive care unit (SICU ) during recent 5 years ,then instruct clinical application of antibiotics reasonably .Methods Abdominal drainage of 65 patients of intra-abdominal infection associated sepsis were collected from January 2008 to December 2012 .All the specimens were analyzed for pathogen distribution and drug susceptibility .Results A total of 151 strains of pathogenic bacteria was isolated ,in which Gram-negative bacteria were the most popular pathogen (104 strains ,68 .9% ) ,whereas Gram-positive bacteria and fungi accounted for 19 .2% (29 strains) and 11 .9% (18 strains) ,respectively . The five most common pathogens were Escherichia coli(23 .2% ) ,acinetobacter baumannii(15 .2% ) ,enterococcus faecium(13 .2% ) , pseudomonas aeruginosa(8 .6% ) ,andklebsiella pneumonia(7 .9% ) .The rate of the ESBL-producing strains of escherichia coli and pneumonia pneumonia were 80 .0% and 33 .3% .Both of them showed low resistance to carbapenem antibiotics .The proportion of multidrug resistantstrains and extensive drug resistant strains of acinetobacter baumannii was 56 .5% and 30 .4% ,respectively .Con-clusion The resistance of the pathogen isolated from the patients of intra-abdominal infection associated sepsis in SICU is seriously high .Early and rational using of antibiotics is of great importance to control the production and transmission of drug resistance .

Objective To observe the stability and the change pattern of VEGF expression in myocardium in varied postmortem periods,and to evaluate its usefulness in diagnosis of early myocardial ischemia after death.Methods An animal model of early myocardial ischemia was established by ligating coronary artery of rabbit,immunohistochemistry(SP protocol),image analysis technique and statistical analysis system are applied to detect and compare the area and intensity of expression of VEGF in cardiocytes,and its stability in different postmortem perieds.ResultsIn ischemic myocardium,VEGF shows foci or sheets of intense positive staining in cardiocytes,with negative or weak staining in some cells.There was weak staining in vascular endothelial cells and smooth muscle cells,but no staining in interstitium.When ischemic myocardium stored at 4℃,the staining of VEGF became weaker with time delay,but there was weak staining in a fraction of cardiocytes even 10d after death.There was significant difference in the intensity of VEGF staining between ischemic and normal postmortem myocardium from 1 to 10d.Conclusion VEGF can withstand a certain degree of autolysis or putrefaction,and the immunohistochemical staining of it is valuable in the diagnosis of early myocardial ischemia in corpses stored at 4℃ for 1~10d after death.

Teaching is very important for anesthesiology developmemt,so residents should be cultivated the teaching capacity as soon as possible.This article discussed how to cultivate the teaching capacity of residents in anesthesiology department.

Objective To study the feasibility of TCI etomidate for total intravenous anesthesia (TIVA). Methods Forty patients scheduled for abdominal operation were divided into two groups with 20 cases each. Anesthesia in group E was induced and maintained with TCI etomidate 1-2 μg/ml and remifentanil 6 ng/ml,which in group P with TCI propofol 2-4 μg/ml and remifentanil 6 ng/ml to keep BIS 40-60. The perioperative changes of plasma glucose, cortisol, aldosterone and ACTH were Observed. Recovery from anethesia was recorded as well Results Both groups had the stabilized hemodynamics and glucose concentration. The plasma cortisol and ACTH concentrations in group E were decreased at the end of operation(P<0.05), but returned to preoperative level on the next day, which were not significantly changed perioperatively in group P. The time of eye opening was longer in group E than that in group P. Conclusion Etomidate has an inhibition on the function of the adrenal cortex temporally and can be used safely togather with remifentanil for TIVA in patients without hypoadrenocorticism.

The metabolic response to stress plays a key role in the adaptive response during critical illness.Multiple mechanisms including the stimulation of the sympathetic nervous system,inflammation,and immune responses were involved.Insulin resistance is one of the main features in metabolic response to stress.Metabolic response to stress was manifested by disorders of energy consumption,such as glucose,lactic acid,lipids,and proteins.The decrease in fat-free body mass and cell mass,relative excess of adipose tissues,and increased extracellular fluid volumes were also involved.Therapeutic interventions,including hormone supplementation,enhanced protein intake,and early mobilization,are considered for prevention and therapy of metabolic response to stress.The review aims to summarize the pathophysiological mechanisms,clinical consequences,and therapeutic implications of metabolic response to stress in critical illness.

Sepsis is a leading cause of death in critically ill patients.The definitions of sepsis and septic shock were introduced in 1991 and last revised in 2001.Since considerable advances had occurred to its pathophysiology and management,an update definitions for sepsis and septic shock were released in February 2016 by the Society of Critical Care Medicine and the European Society of Intensive Care Medicine.This article is to review the development and limitations of previous versions of sepsis definition,and summarize the sepsis 3.0 definition and its clinical diagnosis criteria.These updated definitions and clinical criteria will play vital roles in providing important reference frame for clinical trials,and facilitating early recognition and timely management of patients with sepsis.

Objective To evaluate the role of autophagy in survival of hypoxia-preconditioned bone marrow mesenchymal stem cells (BMSCs) in damaged tissues resulting from spinal cord ischemiareperfusion (I/R) injury in rats.Methods In vitro experiment Rat BMSCs were seeded in 12-well plates at a density of 1× 106 cells/ml (1 ml/well) , and randomly divided into 6 groups (n =30 wells each) : control group (group C) , normoxia-incubated group (group N) , hypoxic preconditioning (HP) group (group H), HP + AMP-activated protein kinase (AMPK) inhibitor Compound C group (group HC), HP + autophagy inhibitor 3-methyladenine group (group HM) and HP + mammalian target of rapamycin (mTOR) inhibitor rapamycin group (group HR).In HC, HM and HR groups, 10 mmol/L Compound C, 5 mmol/L 3-methyladenine and 10 nmol/L rapamycin were added to the culture medium, respectively, at 3 h before HP.Twelve wells in each group were selected, and the expression of phosphorylated AMPK (p-AMPK) , phosphorylated mTOR (p-mTOR), microtubule-associated protein 1 light chain 3 Ⅰ (LC3 Ⅰ), and LC3 Ⅱ in BMSCs was determined.Eighteen wells in each group were selected, and BMSCs were co-cultured with 500 μ mmol/L H2O2 for 24 h, the survival and apoptotic rate of BMSCs were measured, and the activities of caspase-9 and caspase-3 were detected.In vivo experiment Adult male Sprague-Dawley rats, weighing 300-350 g, aged 3 months, underwent spinal cord I/R.A total of 192 rats with spinal cord I/R injury were randomly divided into C, N, H, HC, HM and HR groups (n =32 each) using a random number table.At 30 min of reperfusion, BMSC suspension 5 μ l (1×106 cells/ml) processed in N, H, HC, HM and HR groups of in vitro experiment was implanted into the lumbar segment (L1-5) of the spinal cord in N, H, HC, HM and HR groups, respectively.Neurological function was scored at 4, 12, 24 and 48 h of reperfusion.The lumbar segment of spinal cord was removed for detection of apoptosis in BMSCs.Results In vitro experiment Compared with group N, the p-AMPK expression, LC3 Ⅱ/LC3 Ⅰ and survival rate were significantly increased, and p-mTOR expression, apoptotic rate and activities of caspase-9 and caspase-3 were decreased in group H (P＜0.05).Compared with group H, the p-AMPK expression, LC3 Ⅱ/LC3 Ⅰ and survival rate were significantly decreased, and p-mTOR expression, apoptotic rate and activities of caspase-9 and caspase-3 were increased in group HC, LC3 Ⅱ/LC3 Ⅰ and survival rate were decreased, and apoptotic rate and activities of caspase-9 and caspase-3 were increased in group HM, and p-mTOR expression, apoptotic rate and activities of caspase-9 and caspase-3 were decreased, and LC3 Ⅱ/LC3 Ⅰ and survival rate were increased in group HR (P＜0.05).In vivo experiment Compared with group N, the neurological function scores were significantly increased, and the number of apoptotic BMSCs was decreased in group H (P＜0.05).Compared with group H, neurological function scores were significantly decreased,and the number of apoptotic BMSCs was increased in HC and HM groups (P＜O.05).Conclusion Enhanced autophagy is involved in survival of hypoxia-preconditioned BMSCs in damaged tissues resulting from spinal cord I/R injury, and the mechanism is associated with activated AMPK/mTOR pathway in rats.

Objective To investigate the feasibility of repairing spinal tracts with peripheral nerve graft combing neurotrophic factors in rats following complete spinal cord transection.Methods One hundred and twenty-one male Wistar Rats were transection at T9 level of spinal cord, and randomly divided into five groups. Group A with spinal cord transection was underwent acidic fibroblast growth factor (aFGF) treatment and peripheral nerve grafts (n=25); Group B: spinal cord transection was underwent aFGF treatment only (n=25); Group C: spinal cord transection was underwent peripheral nerve grafts only (n=25); Group D: spinal cord transaction only (n=25); and Group E: sham control (laminectomy only, n=21). The locomotor behavior of all rats was analyzed by the BBB open field locomotor test over the six months of survival time. Motor evoked potentials (MEP) were used to evaluate axon growth across the damage site. Biotinylated Dextran Amine (BDA) and retrograde tracing with fluorogold were used to evaluate the presence of axons through the damage site after treatment. Results The presence of anterograde BDA labeling of corticospinal tract axons at the graft site and fluorogold retrograde labeling of neuron populations was found in motor cortex and in red nucleus, reticulospinal nuclei, raphe nuclei, and vestibular nuclei in Group A. The average latency and amplitude of MEP were improved significantly in Group C. The mean of BBB scores showed significant improvement in Group A. Statistical analysis indicated that Group A had significant improvement compared to Group BC and D at 6 months post-surgery (P

Objective The purpose of this study was to investigate the effect of isoflurane on baroreflex sensitivity ( BRS ) during induced hypotension and to illucidate the mechanism of isoflurane-induced hypotension. Methods Fifteen female ASA I or II patients aged 13-16 yrs undergoing scoliosis surgery were studied. The patients were unpremedicated. Radial artery and internal jugular vein were cannulated for BP and CVP monitoring. EGG, BP and SpO2 were continuously monitored before and during anesthesia. Anesthesia was induced with midazolam 0.04 mg? kg-1 , fentanyl 2 ?g? kg-1 and propofol 2 mg? kg-1 . Tracheal intubation was facilitated with rocuronium 1 mg?kg-1 . Anesthesia was maintained with isoflurane inhalation and fentanyl infusion (0.4?g?kg-1?h-1). Nitroglycerin (NTG) was infused at 1 ?g?kg-1 ?min-1 at the beginning of surgery to control MAP at 55-65 mm Hg and esmolol 20 mg was given i. v. to control HR 0.8. BRS was measured before induction of anesthesia (T1), immediately after intubation (T2), when end-tidal concentration of isoflurane reached 0.7% (T3 , supine) (T4 , prone), when end-tidal concentration of isoflurane reached 1.3% (T5) , at 30 min after NTG infusion and esmolal bolus injection were stopped (T6) when end-tidal concentration of isoflurane was decreased to 0.7 % (prone, T7 ) and immediately after the patients were turned supine (T8 ) . Results When end-tidal isoflurane concentration reached 1.6%, the desired level of hypotension could be maintained without NTG infusion and esmolol injection. BRS gradually decreased with increasing end-tidal isoflurane concentration. BRS was the lowest at 30 min after termination of NTG infusion and esmolol bolus injection. Conclusion Isoflurane depresses BRS and BRS depression may be involved in the mechanism of isoflurane-induced hypotension.

Objective To investigate the effect of midazolam on expression of adhesion molecules on the platelet membrane surface in patients with coronary heart disease (CHD) .Methods Blood samples were taken from 10 healthy volunteers and 40 patients with CHD and anticoagulated with 3.8% sodium citrate. Platelet rich plasma (PRP) was obtained by centrifugation at 800 r/min for 8 min at room temperature. Ten volunteers served as control group (group E). The 40 patients with CHD were randomly divided into 4 groups ( n = 10 each) : group A, B, C and D. In group E and group A PRP was incubated without midazolam while in group B, C and D PRP was incubated with midazolam 100 (B) , 200 (C) and 400 ng?ml-1 (D) for 3 min. The inhibitory effect of midazolam on expression of CD154, CD41/61 and CD26p on the platelet membrane surface was determined by flow cytometry. Results The five groups were comparable with respect to age, sex (M/F ratio) , body weight, platelet count, bleeding and coagulation time. The expression of CD154, CD41/61 and CD62p on the platelet surface was significantly increased in patients with CHD. Midazolam 200 and 400 ng?ml-1 inhibited the expression of CD154, CD41/61 and CD62p on the platelet membrane surface in patients with CHD, whereas midazolam 100 ?g?ml-1 had no significant effect on CD154, CD41/61 and CD62p. Conclusion The expression of adhesion molecules on the platelet membrane surface is greater in patients with CHD than in healthy adults. Midazolam 200 and 400 ng?ml-1 can inhibit the expression of CD154, CD41/61 and CD62p on the platelet membrane surface.