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.

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.

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.

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.

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.

Recent evidence suggests Toll like receptor 4 (TLR4) and its accessory protein MD2 mediate endotoxin/lipopolysaccharide (LPS) signaling. LPS binds to LPS binding protein (LBP) in plasma and is delivered to CD14. Next, LPS is transferred to TLR4 MD2 complex. LPS activates several intracellular signaling pathways that include the NF ?B pathway and three mitogen activated peotein kinase (MAPK) pathway: extracellular signal regulated kinase (ERK), c Jun N terminal kinase (JNK) and p38. These signaling pathways in turn activate NF ?B and AP 1 (c fos/c jun), which coordinate the induction of many genes encoding inflammatory mediators. Targeting the signaling molecule in the pathway will develop new remedies for treatment of inflammatory disorder.

Objective To observe the protective effect of recombinant human endotoxin binding peptide (EBP) on a rat model of burn combined with endotoxemia. Methods A total of 78 rats of model of burn combined with endotoxemia were divided into three groups: model group ( n =36), treatment group ( n =36), and control group ( n =6). Rats in the model group were intraperitoneally injected with 1 mg/kg endotoxin (prepared with 1 ml saline) immediately after burn. After intraperitoneal injection of 1 mg/kg endotoxin (prepared with 0.5 ml saline), rats in the treatment group were intraperitoneally injected with EBP (prepared with 0.5 ml saline). Blood and liver and lung tissues of rats in the model and treatment groups were collected at 1, 3, 6, 12, 24, and 48 h after treatment. Rats in the control group were intraperitoneally injected with 1 ml saline after trichomadesis. Blood and liver and lung tissues of rats in the control group were collected for the total control. The changes of alanine aminotransferase (ALT), TNF ?, and IL 6 contents in serum were determined by biochemical velocity analysis, ELISA, and light microscopy. The pathological changes of the liver and lung tissues were observed light microscopically and electron microscopically. Results The serum TNF ? level of rats in the model group was significantly higher than that in the control at 1 h after injury ( P