Objective To evaluate the accuracy of monitoring the neuremuscular blockade intraoporatively by transcutaneous electrical stimulation at the P6 acupuncture point. Methods Thirty-five patients, ASA Ⅰ - Ⅲ, BMI≤35 kg/m2 scheduled for abdominal surgery were selected. Anesthesia was induced by sufentunil 0.2-0.3 μg/ kg iv, propofol 2,5-3.5 mg/kg iv. Neuromuscular monitoring was performed by TOF Watch SXR at the P6 acupuncture point on the left forearm and ulnar nerve on the right. The current intensity and gain were recorded frem all the patients;onset time, recovery time of TOF ratio 25% and TOF ratio 90% of atrucurium were also obtained by TOF stimulation on the P6 acupuncture point and the ulnar nerve in patients who were administered a single bolus of atracurium 0.5 mg/kg iv during operation. Controlled ventilation commenced after endotracheal intubation. Results There were no significant differences between the P6 acupuncture point and the ulnar nerve in stimulus intensity or gain ( P > 0.05 ). There were no significant differences between the P6 acupuncture point and the ulnar nerve in onset time, recovery time of TOF ratio 25% and TOF ratio 90% (P > 0.05).Conclusion Transcutaneous electrical stimulation at the P6 acupuncture point can be used to monitor neuromuscular blockade intraoperafively.

Objective To investigate the protective effects of Shenfu injection on myocardium against ischemia and reperfusion injury in rats. Methods Twenty-four healthy male SD rats weighing 230-280 g were randomly divided into three groups (n = 8,each): sham-operation group(Sham), ischemia and reperfusion group (I/R), Shenfu injection group(SF) . In Sham group, the anterior descending branch of left coronary artery was exposed and a piece of silk thread was placed around the artery but untied. The ischemia and reperfusion injury models in I/R and SF groups were made by temporary ligation of the anterior descending branch of left coronary artery,ischemia lasted for 30 min and reperfusion for 60 min. In SF group, the Shenfu injection(10 ml/kg) was intraperitoneally injected 30 min before ischemia. In Sham and I/R groups, normal saline (10 ml/kg) was intraperitoneally injected. After 60 min reperfusion, the blood samples of all rats in each group were collected from the left carotid arterial catheter for determination of the concentrations of plasma TNF-?, IL-6 ( ELISA) . The myocardium samples were obtained for ultrastructure observation (Electron-microscope) .Results Compared with that in Sham group, the plasma concentrations of TNF-? and IL-6 in I/R group significantly increased( P

Objective To investigate the effect of angiotensin Ⅱ type Ⅰ receptor antagonist losartan on the infarct size and ultrastructure of myocardium and activation of NF-?B induced by myocardial ischemia and reperfusion (I/R) and the possible underlying mechanism. Methods Forty-two healthy male SD rats weighing 215-285 g were randomly divided into 4 groups: in control group ( n = 6) the anterior descending branch of left coronary artery (LCA) was exposed but not occluded; in I/R group (n = 12) the anterior descending branch of LCA was occluded for 30 min followed by 60 min reperfusion; in group LOS1 ( n = 12) and group LOS2 ( n = 12) losartan 5 mg (LOS1) or 10 mg (LOS2) was injected i.v. 15 min before myocardial ischemia. At the end of 60 min reperfusion the animals were killed and the hearts were harvested for determination of (1) myocardial infarct size (by TTC) , (2) ultrastructure of myocardium (electron microscope) and (3) activation of NF-?B.Results The infarct size in group LOS1 (34.6%?2.2%) and LOS2 (21.8%?4.0%) was significantly smaller than that in I/R group (45.4%?2.4%). Myocardial ultrastructure was well preserved in group LOS1 and LOS2 as compared to I/R group. NF-?B activity was significantly increased in I/R group and losartan pretreatment significantly reduced the increase in NF-?B induced by I/R. Conclusion Angiotensin Ⅱ type Ⅰ receptor antagonist losartan has cardioprotective effect on myocardium against I/R in a dose-dependent manner. Modulation of NF-?B activated by I/R may be involved in the mechanism.

Objective To investigate the effects of thiopental on expression of nuclear factor kappa B (NF-?B) and content of TNF-? and IL-1? in the lungs induced by lipopolysaccharide (LPS) .Methods Twenty-four male Kunming mice weighing 15-25 g were randomly divided into 4 groups (n = 6 each) : I control group received intraperitoneal (i.p.) normal saline (NS) 1 ml?kg-1 ; Ⅱ LPS group received i.p. LPS 5 mg?kg-1 ; Ⅲ LPS + thiopental (TH) received intrapentoneal TH 60 mg?kg-1 20 min after i.p. LPS 5 mg?kg-1 and Ⅳ TH group received i.p. TH 60 mg?kg-1 alone. The animals were bled to death at 3 h after LPS administration. The lungs were immediately removed for determination of expression of NF-?B p65 (Western blot) and TNF-? and IL-1? content (ELISA) in the lung. Results The expression of NF-?B p65 was significantly increased and the level of TNF-? and IL-1? in the lungs were significantly increased after LPS stimulation as compared with control group ( P

Objective To study the molecular biological mechanism of the protective effect of angelica on myocardium during ischemia reperfusion Methods The myocardial ischemia/reperfusion was induced with the 40 min cross clamp/120 min declamping of anterior decending coronary artery Forty SD rats were randomly divided into 3 groups: group A without myocardial ischemic reperfusion , group B with intravenous adminisrtration of normal saline 0 8ml/100g before ischemia reperfusion , and group C with intravenous adminisrtration of 25% angelica 0 8ml/100g before ischemia reperfusion The content of protein kinase C (PKC) in cardiac myocyte was measured with immunohistochemical method, and the PKC activity with the isotope lable method Results Compared with those in group B, the myocardial infarct size reduced significantly in group C (P0 05) but increased obviously in group C (P0 05) The PKC activity was significantly higher in group C than that in group A(P

ve To investigate the effect of intravenous cAMP on the myocardial infarct size, the ultrastructure of myocardium and myocardial cell apoptosis and the possible mechanism of myocardial protection affected by cAMP against ischemia /reperfusion (I/R) injury. Methods Forty SD rats of either sex weighing 250-280g were anesthetized with abdominal sodium pentobarbital 4.5mg/100g, tracheotomized and mechanically ventilated (VT = 2ml/100g, RR = 60bpm) . Myocardial I/R was produced by tying and untying of left anterior descending coronary artery. Ischemia lasted 30 min and reperfusion 2h. Rats were randomly divided into 3 groups: control group (n = 8) in which left anterior descending coronary artery was exposed and a piece of silk thread was placed around the artery but not tied; I/R group (n = 16) in which normal saline 1ml was injected into sublingual vein before I/R; cAMP group (n = 16) received intravenous cAMP 1mg/kg 5min before I/R. The animals were then sacrificed and heart was harvested for determination of myocardial infarct size (by TTC) and ultrastructure examination (electron microscope) . Apoptosis was identified by TUNEL and apoptosis index (AI) was obtained. The expression of Fas, Bcl-2 protein was measured by immunohistochemical technique. Results The infarct size was smaller in cAMP group than that in I/R group . Myocardial apoptosis and necrosis were quite obvious in I/R group whereas in cAMP group the ultrastructure of myocardium was fairly normal. The AI in I/R group was significantly higher than that in cAMP group (P 0.05 ) . Conclusions cAMP can protect myocardium from I/R injury by modulating the expression of Fas and Bcl-2 protein and inhibit apoptosis following myocardial I/R.

Objective To investigate the protective effects of different concentrations of propofol on thelungs apainst acute injury induced by lipopolysaccharide (us) in rats.Methods Twenty-four male Wistar ratsweighing 150-250g were randomly divided into 4 groups with 6 animals in each group : (1) control group receivedonly normal saline; (2) LPS group received LPS 5 mg?kg~(-1)i. v.; (3) propofol group 1 received a bolus 5 mg?kg~(-1) after LPS followed by propofol infusion at 5 mg?kg~(-1) ; (4) propofol group Ⅱ received a bolus of propofol 10mg.kg~(-1) after LPS followed by propofol infusion 10 mg?kg~(-1). Blood samples were obtained from femoralartery for determintiion of serum concentrations of TNF-?, IL-? and IL-10 at 1, 2, 3, 4 h after LPS injection. Theanimals were then killed by exsanguination. The lungs were removed. Left lung was lavaged and the broncho-alveolar lavage fluid (BALF) was collected for determination of its neutrophil count, and protein, TNF-?, IL-I?and IL-10 levels. Right lung was used for measurement of wet / dry lung weight ratio. Results In LPS group thewet/dry lung weight ratio, BALF neutrophil counts and protein contents and BALF and serum TNF-?, Ib-I? andIL-10 levels were significantly increased compared with control group (P

Objective Ketamine has been shown to suppress pro-inflammatory cytokines like TNF-? and IL-6. The purpose of this study was to investigate the effects of ketamine on myocardial NF-?B expression and serum IL-6 level in a rat model of myocardial ischemia-reperfusion (I/R) .Methods Twenty-four healthy male SD rats aged 4-8 months weighing 200-250 g were randomly divided into four groups with 6 animals in each group : (A)control group; (B) I/R group; (C) ketamine 5 mg? kg-1 +I/R(I/R+K1) and (D) ketamine 10mg?kg-1 + I/R (I/R + K2) . The animals were anesthetized with intraperitoneal 10% chloral hydrate 40 mg?kg-1. Chest was opened and heart exposed. Left coronary artery was temporarily occluded at 1 mm inferior to left auricle for 30 min followed by 120 min reperfusion. Myocardial ischemia was confirmed by decoloration of apex and elevation of S-T segment. In control group (A) heart was exposed but left coronary artery was not occluded. In group C and D ketamine 5 mg?kg-1 or 10mg?kg-1 was given i.v. during ischemia. The animals were sacrificed at the end of 120 min reperfusion. A piece of myocardium (0.1 g) was obtained from apex for determination of myocardial NF-?B expression (Western-blot) . Blood samples were taken at 30 min and 120 min of reperfusion for determination of serum IL-6 level (ELISA) .Results The serum IL-6 level at 30 min and 120 min of reperfusion and myocardial NF-?B expression were significantly increased in I/R group (B) compared with those in control group ( P

AIM: To study the protective effects of shenfu injection on myocardial ischemia/reperfusion (I/R) injury in rats and its potential mechanisms. METHODS: Myocardial ischemia/reperfusion was produced by tying and untying of left anterior descending coronary artery. Ischemia lasted for 30 min and reperfusion for 60 min. Twenty-four healthy male SD rats weighing 230-280 g were randomly divided into three groups (n=8 in each): sham-operation group, I/R group, and shenfu group which the shenfu injection (10 ml?kg -1) were injected intraperitoneally 30 min before ischemia. The plasma concentration of tumor necrosis factor-? (TNF-?), interleukin-6(IL-6) were measured by ELISA. The heart was harvested and levels of the nuclear factor kappaB (NF-?B) activity were determined by Ecl-western blot analysis and ultrastructures were observed by electron microscopy. RESULTS: NF-?B binding activity in myocardial nuclear and the plasma concentration of IL-6, TNF-? were significantly increased in I/R group than that in the sham-operation group (P

Objective To replace the endogenous CTL epitope LLD in HBsAg with EYILSLEEL of glypican(GPC3)in order to prepare a GPC3-HBsAg multiple peptides vaccine for HBV infection.Methods The HBsAg/GPC3 DNA was amplified by gene splicing by overlap extension(SOEing)PCR from pcHBsAg plasmid and then inserted into pBSSK+ vector to construct a pBSSK/GPC3 vector.The vector was then identified by PCR,double digesting and sequencing.The fragment encoding GPC3 CTL epitope EYILSLEEL was obtained by double digesting the plasmid pBSSK/GPC3 and then inserted into pcDNA3.1+ vector.Results Sequencing and restrict endonulease digestion indicated that eukaryotic expression vector pcDNA-HBsAg/GPC3 was constructed successfully.Conclusion The endogenous CTL epitope LLD of HBsAg is replaced by the EYILSLEEL,and an eukaryotic expression vector pcDNA-HBsAg/GPC3 is constructed.