Objective To explore the effects of levosimendan on hemodynamics and activated level of HIF-1 in patients with coronary heart disease and heart failure.Methods 80 patients with coronary heart disease and heart failure in our hospital were selected as the research subjects,they were randomly divided into two group,40 cases in each group.The control group received routine treatment,the observation group was given conventional treatment combined with levosimendan.The clinical efficacy,the occurrence of adverse reactions,hemodynamic parameters and HIF-1 alpha activation level were compared between the two groups.Results The total effective rate in the observation group was 95.00％,which was higher than 80.00％ in the control group(x2 =4.114,P ＜0.05).After treatment,left ventricular ejection fraction(LVEF),stroke volume (SV),HIF-1 alpha activation levels in the observation group were (49.36 ± 3.65) ％,(76.29 ± 5.31) mL and (0.47 ± 0.15),compared with before treatment,LVEF and SV were significantly higher(t =14.998,10.267,all P ＜ 0.05),HIF-1 alpha activation level was significantly lower (t =9.624,P ＜ 0.05),and compared with the control group after treatment,the differences were statistically significant(t =8.264,4.726,4.411,all P ＜ 0.05).The two groups had no obvious adverse reactions.Conclusion Levosimendan in the treatment of coronary heart disease and heart failure has significant clinical efficacy,can effectively improve the hemodynamics and cardiac function in patients,also can inhibit HIF-1 alpha level,it is safe and reliable.

Aim Cerebral ischemic tolerance can be induced by a variety of preconditioning stimuli,such as transient global and focal ischemia,hypoxia,and administration of lipopolysaccharide(LPS),proinflammatory cytokines,anesthetics.Tolerance can be established with two forms: a rapid form in which the trigger induces tolerance to ischemia within minutes and a delayed form in which development of protection takes several hours or days.During ischemia,inflammatory reaction was initiated by toll-like receptors(TLRs) that recognize host-derived molecules released from injured tissues and cells,which exacerbates ischemic injury.In the delayed form of tolerance,the preconditioning stimuli first triggers the TLRs inflammatory pathway,leading not only to inflammation but also to simultaneous upregulation of feedback inhibitors(such as anti-inflammatory cytokines,decoy receptors,and signaling inhibitors),which reduced the inflammatory response to subsequent severe ischemia.The rapid tolerance is achieved by direct interference with membrane fluidity,causing change of lipid rafts leading to inhibition of TLRs signaling pathways.The comprehension of mechanism of cerebral ischemic tolerance highlights new avenues for future prevention and treatment of ischemic brain injury

To observe the effects of polyclonal antibodies to rat LPS binding protein on LPS induced activation of NF ?B and production of TNF ? and IL 6 in the lung. The activation of NF ?B and the contents of TNF ? and IL 6 were measured by electrophoretic mobility shift assay and ELISA respectivly. We found that both the activity of NF ?B and the levels of TNF ? and IL 6 in the lung were significantly decreased by the antibodies when used at early stage, but not at late stage after LPS challenge. These data indicated that the antibodies to LPS binding protein might have a potential value in the prevention of acute lung injury as a result of LPS challenge.

To explore the effects of lipopolysaccharide binding protein (LBP) on toll like receptor 4 (TLR4) pathway in alveolar macrophages of acute lung injury induced by lipopolysaccharide (LPS) in rats. The TNF ?concentration, IL 1? and IL 18 mRNA expression in alveolar macrophages (AM?) from rats challenged with LPS or LPS + LBP or LPS+LBP+multi LBP antibody (mLBPab) were measured with ELISA and semi quantative reverse transcription polymerase chain reaction (RT PCR) respectively. The expression of TLR4 was determined with RT PCR and Western blot. The results showed that: the TNF ? concentration ,IL 1?, IL 18 mRNA expressions and TLR4 expression were increased significantly in the AM? stimulated with LPS +LBP compared with single LPS stimulation group. However, mLBPab blocked these effects. It is suggested that LBP could enhance the trans membrane transduction function of LPS via TLR4 in rat AM? and these might be the main reason that LBP could enhance the inflammatory activity of LPS, and LBP antibody could be used to alleviate such morbid conditions such as SIRS, acute lung injury, ARDS, and septic syndrome.

0.05) at 3, 30 and 90 days after operation. The differences of ESVI, EDVI, LVEF and WMSI were significant between 30d,90d and 3d in every group(P

Objective To explore the effect of isoflurane on Na-K-ATPase activity in cultured primary alveolar type Ⅱ(ATⅡ) cells with or without being injured by H 2O 2.Methods ATⅡcells were isolated from adult rat lungs and incubated for 24h and divided into six groups. Group 1 served as control and received no treatment. Group 2 and 3 ATⅡ cells were exposed to 0.28 or 2.8mmol/L isoflurane. In group 4 cells were exposed to 75?mol/L H 2O 2. In group 5 and 6 cells were exposed to both 75?mol/L H 2O 2 + 0.28 or 2.8mmol/L isoflurane. Each group was incubated for another 2h after the addition of isoflurane and /or H 2O 2. The Na-K-ATPase activity of ATⅡcells ,the LDH activity and the MDA concentration of fluid culture medium were measured by biochemical methods.Results Isoflurane markedly decreased Na-K-ATPase activity in normal ATⅡ cells, but aggravated the decrease in Na-K-ATPase activity induced by H 2O 2. Isoflurane had no effect on LHD activity and MDA concentration of fluid culture medium of normal ATⅡ cells ,but significantly increased LHD activity and the MDA concentration of of fluid culture medium of ATⅡ cells injured by H 2O 2.Conclusions Isoflurane can inhibit Na-K-ATPase activity of ATⅡ cells in vitro, and aggravate the damage of ATⅡ cells caused by oxidants.

AIM To determine the effect of isoflurane(Iso) on pulmonary surfactant(PS) synthesis in cultured primary ATⅡ cells. METHODS ATⅡ cells were isolated from adult rat lungs and used for the experiments after 32 h in primary culture. Iso 0.28 and 2 8 mmol?L -1 was added into the media of normal and H 2O 2 (75 ?mol?L -1 )-treated cells, and the cells were further incubated for 2 h. The cell proliferation was measured with MTT method and PS synthesis with 3H-choline chloride incorporation. RESULTS Iso had no effect on the proliferation of ATⅡ cells, but markedly decreased PS synthesis in normal alveolar type Ⅱ cells, and aggravated the decrease of PS synthesis induced by H 2O 2. CONCLUSION Iso may decrease PS synthesis of alveolar type Ⅱ cells in vitro , and aggravate the damage of the cells under peroxidation condition.

Objective To Discuss the Clinical Recognition of Acute Myocardial Infarction(AMI) caused by aortic valve incompetence.Methods Data of 275 AMI patients in our hospital recent two years,7 of them were caused by aortic valve incompetence; all of patients(7 AMI) were received coronary artery angioplasty,ultrasound,left ventricular angiography examination,its clinical feature was analyzed.Results All of 7AMI patients have normal coronary without limited constriction or plaque and with aortic valve incompetence.

Objective To observe effects of the antisense genes of Toll-like receptor 4 (TLR4 ) and myeloid differentiation protein-2 (MD2) on the activation of NF-?B in alveolar typeⅡepithelial cells (ATⅡcells) induced by lipopolysaccharide (LPS). Methods Cultured ATⅡcells were randomized to normal cells (control) group,LPS group,LPS+empty vector group,LPS+TLR4 antisense gene group,LPS+MD2 antisense gene group,LPS+TLR4-MD2 antisense gene group. The expressions of TLR4 and MD2 mRNA and protein in ATⅡcells were detected by Northern blotting and Western blotting respectively. The activity of NF-?B in ATⅡcells was measured with electrophoretic mobility shift assay (EMSA). The TNF-? and IL-6 concentrations in the supernatant of cultured ATⅡcells were tested with ELISA.Results Compared with control groups,the expressions of TLR4 and MD2 mRNA and protein,the NF-?? activity,the levels of TNF-? and IL-6 were increased remarkably in LPS group and LPS+empty vector group (P

Objective To investigate the effect of dexmedetomidine on patients with pancreatic cancer treated by high intensity focused ultrasound (HIFU) under general anesthesia.Methods One hundred and twenty ASA Ⅱ or Ⅲ patients with pancreatic cancer undergoing HIFU treatment,were divided into control group (group C) and dexmedetomidine group (group D) by random digits table method,each group with 60 cases.Dexmedetomidine was intravenously infused at 0.2 μ g/(kg· h) until the end of operation after a loading dose of 0.7 μg/kg over 15 min before induction of anesthesia in group D,while the equal volume of normal saline was infused in group C.Anesthesia was induced with intravenous injection of fentanyl 2-3 μg/kg and propofol 1.5-2.0 mg/kg and cisatracurium 0.2 mg/kg at 5 min after administration of the loading dose.Anesthesia was maintained with sevoflurane,remifentanil,propofol,cisatracurium.The propofol,remifentanil and sevoflurane consumption,the incidence of postoperative agitation,delirium,delayed recovery were recorded.Results The intraoperative heart rate in group D was significantly lower than that in group C (P ＜ 0.05).The propofol,remifentanil and sevoflurane consumption in group D were significantly shorter than those in group C [(341.4 ± 45.7) mg vs.(520.5 ± 50.8) mg,(1.7 ± 0.5) mg vs.(2.3 ± 0.8) mg,(11.6 ± 4.1) ml vs.(16.7 ± 3.8) ml,P ＜ 0.05].The incidence of postoperative agitation and delirium in group D were significantly lower than those in group C [6.7％(4/60) vs.21.7％(13/60),8.3％ (5/60) vs.26.7％ (16/60),P ＜ 0.05].There was no statistically significant difference in the incidence of delayed recovery between group D and group C [3.3％ (2/60) vs.1.7％ (1/60),P ＞ 0.05].Conclusions Dexmedetomidine given HIFU treatment of pancreatic cancer patients can reduce the amount of general anesthetic,reduce the incidence of postoperative agitation and delirium,intraoperative heart rate.