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Objective@#To investigate the early intervention effects of metoprolol on connexin 43(Cx43) and phosphorylated Cx43 (p-Cx43) expression in rabbits with post myocardial infarction.@*Methods@#A total of 24 adult male New Zealand white rabbits were divided into sham group (n=6), early treatment group(n=6), routine treatment group(n=6), and myocardial infarction group(n=6) with a randomized block design blocked by weight. Myocardial infarction was induced by left anterior descending coronary artery (LAD) ligation. Rabbits in sham group received similar surgical procedure without LAD ligation. Metoprolol (12.5 mg/kg dissolved in 2 ml distilled water) was applied to rabbits in early treatment group and routine treatment group per gavage immediately after recovery from anesthesia and at 24 hours after myocardial infarction, respectively, then treated daily for 40 days. Rabbits in sham group and myocardial infarction group received 2 ml distilled water per gavage daily for 40 days. Plasma lactate dehydrogenase (LDH) and creatine kinase (CK) level were detected by automatic biochemistry analyzer after 6 hours in all rabbits. Ventricular fibrillation threshold (VFT) was measured in vivo by bipolar pacing electrodes at 40 days. Cx43 and p-Cx43 distribution in ventricular tissue was detected by immunofluorescence analyses. Cx43 and p-Cx43 protein level in ventricular tissue was determined by Western blot.@*Results@#(1) Plasma LDH ((851.7±85.9)U/L vs. (332.3±39.6)U/L, P<0.01) and CK ((1 192.7±105.3)U/L vs. (462.3±65.6)U/L, P<0.01) were significantly higher in myocardial infarction group than in sham group (both P<0.01). (2) VFT was significantly lower in myocardial infarction group than that in sham group ((470.0±91.0) beats per minute vs. (683.3±60.9) beats per minute, P<0.05), and VFT was significantly higher in early treatment group ((633.3±43.2) beats per minute) and routine treatment group ((645.0±30.8) beats per minute) than in the myocardial infarction group (both P<0.05). (3) Immunofluorescence analyses showed that Cx43 was mainly localized in the intercalated disk, which was perpendicular to the cell long axis with linear arrangement, and less lateral distribution in sham group, early treatment group and routine treatment group, which was significantly different as the case in the myocardial infarction group. The expression of p-Cx43 in myocardial infarction group was less than in sham group, which was significantly upregulated in in early treatment group and routine treatment group when compared with myocardial infarction group, and expression of p-Cx43 was significantly higher in early treatment group than in routine treatment group. (4)The p-Cx43/Cx43 ratio of protein was significantly lower in myocardial infarction group than in sham group (0.165±0.011 vs. 0.363±0.046, P<0.05), and significantly higher in early treatment group (0.720±0.063) and routine treatment group (0.364±0.030) than in myocardial infarction group (both P<0.05), and this ratio was significantly higher in early treatment group than in routine treatment group (P<0.05).@*Conclusion@#Metoprolol treatment, especially the early metoprolol treatment (within 24 hours after LAD ligation), could significantly improve VFT by ameliorating the distribution and dephosphorylation of myocardial Cx43 in rabbits with experimental myocardial infarction.
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Objective: To investigate the role of aldehyde dehydrogenase-2 (ALDH-2) for regulating human endothelial progenitor cells (EPCs) oxidative stress reaction and its mechanism. Methods: Human EPCs were isolated from peripheral blood of healthy adults and the cells were cultured in 4 groups:①Blank control group,②Alda-1 group, the cells were treated by 1μmol/L Alda-1, a speciifc activator of ALDH-2,③tBHP (10μg/ml) group and④Alda-1 pretreatment+tBHP group. EPCs reactive oxygen species (ROS) levels were evaluated by DCFH-DA staining, mitochondrial membrane potentials were detected by JC-1 method, migration capacity was measured by transwell chamber method and the activation of p38 signal pathway was examined by Western blot analysis. Results: Compared with Blank control group, ROS levels in tBHP group and Alda-1 pretreatment+tBHP group were (441.7 ± 24.8) % and (237.4 ± 12.0) %, allP<0.05. In Blank control group, tBHP group and Alda-1 pretreatment+tBHP group, the proportion of EPCs lost their mitochondrial membrane potentials were (5.7 ± 2.1) %, (81.7 ± 3.7) % and (37.4 ± 3.2) % respectively, allP<0.05; the number of EPCs migration were (108 ± 9)/HP, (22 ± 4)/HP and (67 ± 7)/HP respectively, allP<0.05. Compared with Blank control group, the activation of p38 signal pathway increased to (259.1 ± 7.7) % in tBHP group, while it was reduced to (186.4 ± 8.0) % in Alda-1 pretreatment+tBHP group. Conclusion: ALDH-2 could reduce ROS level in human EPCs, it may decrease mitochondrial membrane damage, protect migration which might be related to p38 signal pathway.
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Objective To investigate the effect of norepinephrine (NE) on the proliferation and migration capacity of endo‐thelial progenitor cells (EPCs) ,and bone marrow mobilization and to analyze its molecular mechanism .Methods The 8‐week old C57 mice were taken and randomly divided into 3 groups ,5 cases in each group :the blank control group(subcutaneous injection of normal saline without operaion) ,model group(subcutaneous injection of normal saline and ischemia in left lower extremity ) and NE group(subcutaneous injection of NE 100μmol/100 μL and ischemia in left lower extremity) .The limb ischemia model was prepared by adopting the femoral arterial ligation in mouse left lower extremity ,then NE was continuously pumped by the micro‐osmotic pump .The EPCs contents from bone marrow ,peripheral blood and spleen were assayed with the flow cytometric analyzer ;human peripheral blood EPCs were cultured and stimulated by NE .The proliferation and migration capacity ,and the activation situation of Akt and eNOS signal pathway were detected .Results NE could promote the mobilization of bone marrow EPCs in limb ischemia mice ,increased the EPCs quantity of peripheral blood and spleen ,comparing the NE group with the model group ,the EPCs quantity was increased for bone marrow [(3 .271 ± 0 .772)% vs .(1 .320 ± 0 .256)% ] ,peripheral circulation[(0 .261 ± 0 .041)% vs .(0 .110 ± 0 .028)% ] and spleen[(4 .671 ± 0 .345)% vs .(1 .880 ± 0 .0 .381)% ] ,the differences were statistically significant (P<0 .01) .NE could promote the proliferation and migration capacity ,moreover could activate the Akt‐eNOS signal pathway in EPCs with a dose dependent manner .Conclusion NE could promote the proliferation and migration of EPCs and mouse bone marrow mobilization via the Akt‐eNOS signal pathway .
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Objective:To study the effect and safety of transradial percutaneous coronary intervention (PCI).Meth-ods:Clinical data of 306 patients,who received PCI in our hospital from Mar 2012 to Jan 2014,were retrospectively analyzed,including radial group (n=153),and femoral group (n=153).Therapeutic effect,time and postoperative complications etc.were compared between two groups.Results:A total of 151 cases completed PCI successfully in radial group,the success rate was 98.7%;a total of 150 cases completed PCI successfully in femoral group,the suc-cess rate was 98.0%,there was no significant difference in success rate of operation between two groups,P >0.05. Compared with femoral group,there were significant reductions in hospitalization time [(8.0±3.5)d vs.(3.5± 1.7)d],treatment cost [(3.74±2.06) × 104 yuan vs.(2.61 ± 1.4) × 104 yuan],P <0.01 both,in incidence rates of postoperative coronary occlusion (3.92% vs.0%),arrhythmia (11.76% vs.1.31%),vascular spasm (6.54% vs.1.96%)and hematoma (7.19% vs.0.65%)etc.in radial group,P < 0.05 or < 0.01. Conclusion:Transradial PCI possesses better effect than that of transfemoral ,and it can reduce hospitalization time,cost and postoperative complications,which is worth extending.
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Objective: To explore influence of long-term oral valsartan-angiotensin II type 1 receptor blocker on ventricular arrhythmia after myocardial infarction (MI) in rabbits and its possible mechanism. Methods: A total of 24 New Zealand rabbits were randomly divided into sham operation group (n=8), MI group (n=8) and valsartan group (n=8) according to number table. Sham operation group only received thoracotomy without ligation of anterior descending branch of left coronary artery (LAD), while MI group and valsartan group received ligation of anterior descending branch of LAD. Valsartan group received valsartan gavage (10 mg•kg-1•d-1) since the second day after operation, three groups all were fed for 12 weeks. Mono active potential (MAP) of left ventricular myocardial cells of subendocardial myocardium（inner layer myocardium）, subepicardial myocardium（outer layer myocardium）and middle layer myocardium were recorded before MI and 12 weeks after MI, and times of provocative malignant arrhythmias were recorded on 12 weeks after MI in three groups. Results: 1. Ventricular tachycardia or fibrillation (VT/ VF) episodes were markedly decreased in VAL group than that in MI group on 12 weeks after MI [(3.1±0.8) vs. (12.7±1.5), P＜0.05]; 2. After MI 12 w, the action potential duration to 90% repolarization (APD90) of three-layer ventricular myocytes in MI group was prolonged than that before MI [（259.2±22.1）ms,（288.0±25.8）ms,（244.6±22.6）ms vs.（230.1±23.2）ms,（244.2±23.4）ms,（229.0±21.7）ms, P＜0.05 or＜0.01]；but there were no significant difference in APD90 of three layers ventricular myocytes between before and after MI in valsartan group (P>0.05 all); Compared with sham operation group and valsartan group, there was significant prolonged in transmural dispersion of repolarization (TDR) [(18.8±6.2) vs. (23.9±7.7) vs. (37.2±10.2), P0.05). Conclusions: Long-term oral valsartan can significantly reduce malignant ventricular arrhythmia incidence in rabbits after MI, which may be related to improving TDR in rabbits after MI.
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Objective To investigate the effect of astaxanthin( ASX)on endothelial progenitor cells( EPCs)injury induced by oxidative stress in vitro and to explore its underlying mechanism. Methods Cultured EPCs isolated from peripheral blood were randomly divided into 5 groups:normal control,model group[ tert-butyl hydroperoxide( tBHP)100μmol·L-1 ],and ASX+tBHPgroups(thecellswerepreconditionedwithASX0.1,1.0,and10.0nmol·L-1,respectively).Thecellviabilitywas measured by MTT method. The level of reactive oxygen species( ROS)was determined by DCFH-DA method. The changes of mitochondrial membrane potential( MMP)and apoptosis ratio were detected by JC-1 method and DAPI method,respectively. caspase-3 activity changes of EPCs were detected. Results The cell viability of EPCs was improved with the increasing concentration of ASX. Compared with the model group[(48. 5±4. 3)%],0. 1,1. 0,10. 0 nmol·L-1 ASX significantly increased the cell viabilities[(57. 6±8. 2)%,(77. 6±7. 5)%,and(85. 3±6. 1)%,P﹤0. 05]. The results of DAPI staining revealed that ASX pretreatment could significantly reduce the apoptotic rate of EPCs. The apoptotic rate of the model group was( 27. 8 ± 3. 2)%,while that of ASX+tBHP groups was[(20. 4±2. 9)%,(14. 9±1. 7)%,and(7. 8±0. 7)%,P﹤0. 05],respectively. The data from caspase-3 activity assay indicated that ASX precondition could also remarkably decrease the caspase-3 activity for EPCs. The caspase-3 activity of the model group was(0. 345±0. 018),while that of the ASX+tBHP group were[(0. 291± 0. 013),(0. 209±0. 004),and(0. 169±0. 013),P﹤0. 05],respectively. In addition,treatment with tBHP resulted in an increase of DCF fluorescence,while ASX precondition could decrease the DCF fluorescence,which suggested the accumulation of intercellular ROS for EPCs. Injury of michondrial membrane resulted in the loss of mitochondrial membrane potential( MMP). The MMP detected by JC-1 method revealed that compared with model group,pretreatment of ASX inversed the reduction of MMP. Conclusion Astaxanthin inhibits endothelial progenitor cell apoptosis induced by oxidative stress through inhibiting ROS production,improving the mitochondrial function and down-regulating caspase-3 activity.
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BACKGROUND:Coronary stent implantation can cause blood vessel damage and wal reconstruction, leading to vascular stent restenosis. Studies have found that visfatin is associated with inflammatory reaction, and exhibits an increased expression at the site of plaque rupture in acute myocardial infarction. OBJECTIVE:To investigate the influence of percutaneous coronary intervention on the levels of visfatin in patients with coronary heart disease. METHODS:Thirty patients with acute myocardial infarction within 12 hours after the onset of the chest pain, 30 patients with unstable pectoris and 30 patients with stable angina pectoris were included. Al patients were successfuly treated by percutaneous coronary intervention. Meanwhile, 30 patients only undergoing coronary angiography but not stenting treatment were selected, and another 30 patients without any treatment served as normal control group. RESULTS AND CONCLUSION:According to enzyme-linked immunosorbent method, the visfatin levels of acute myocardial infarction, unstable angina, stable angina and coronary angiography groups continue to rise at pre-operation, 30 minutes, 6 hours, 12 hours, 24 hours after operation, al of which were higher than that in the normal control group (P < 0.05). The results confirmed that within 24 hours after coronary stent implantation the visfatin levels continue to rise.
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Objective To investigate the percentage of CD4 + C125 +Tregs in peripheral blood of patients with sepsis and its effect on cell immunity so as to unravel the effect of immunomodulatory therapy on it. Method Fourty patients with sepsis in ICU were randomly (random number) divided into experimental group and control group . The patients of experimental group were treated with Ulinastatin and immunoregulation agent (Thymosin αl) as well. The blood specimens were collected just before treatment, 3 days and 8 days after treatment. The percentages of CD4 + CD25 + Tregs and lymphocyte subsets were detected by using FCM (flow cytometry), and TNF-α, IL-6 and IL-10 assayed by using ELISA, and APACHE Ⅱ scores were calculated. Results Before treatment, the percentage of CD4 + CD25 + Tregs increased, and the number of lymphocytes and the percentage of T lymphocytes decreased, especially the CD4 + T lymphocytes and CD4+/CD8+ decreased more markedly, and the levels of IL-6 and TNF-α increased. After treatment,the percentage of CD4+ CD25 + Tregs was decreased, the number of lymphocytes and CD4 +/CD8 + increased, and the levels of APACHE Ⅱ score, IL-6 and TNF-α decreased especially in the experimental group decreased more significantly (P ＜ 0. 05). Conclusions The percentage of CD4 + CD25+ Tregs in peripheral blood can reflect the immune status of patients with sepsis and become a novel indicator to estimate the progress of sepsis, and the immunity and prognosis of patients. Treating the patients with Thymosin αl and Ulinastatin can raise their immunity, decrease the levels of IL-6, TNF-α and APACHE Ⅱ score and improve their prognosis.
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Objective To establish a mini pig model suitable for interventional studies in vivo. Methods The endothelia of unilateral renal arteries in 8 purebred Chinese experimental mini pigs(CEMP)was denuded by inflated balloons after the animals were fed with high cholesterol diet for 13 weeks.The CEMP were fed with h high cholesterol diet continuously till the 40th week.The levels of blood lipid panel and creatinine were tested at week 1,14 and 40.Bilateral renal arteries were examined with intravascular uhrasonography at week 14 and 40.The vessel samples were collected at week 40 and stained with haematoxylin-eosin,Masson trichrome technique, oil O and anti-macrophage immunohistological technique. Results Significant differences of blood lipid panel and creatinine were found between week 1 and week 40.Focal ischemic renal injury could be observed pathologically.Renal arteries of CEMP were suitable for interventional procedure such as angiography and intravascular ultrasonography.Cross-sectional information of vessels could be provided clearly by intravascular ultrasonography and the intimamedian thickness of injured renal arteries was much thicker than that of non-injured ones[(0.89±0.03)mm vs (0.30±0.02)mm,P＜0.05]as evidenced by this diagnostic technique.Pathological findings demonstrated the atheroselerotic profiles of the injured renal arteries.Fibrous and fibro-fatty plaques were the main pathologic types in this CEMP model. Conclusions An animal model with renal arterial atherosclerosis mimicking the progression of atheroselerotic renovaseular disease,which is suitable for interventional procedure is established successfully.Intravascular ultasonography may have potential clinical prospect on the evaluation of atherosclerotic renovaseular disease.
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Objective To explore the predisposing factors in the development of acute respiratory failure after abdominal surgery and the factors affecting the therapeutic effect of mechanical ventilation. Methods A (retrospective) study was undertaken for acute respiratory failure after abdominal surgery in 91 patients. The (underline) diseases, introducing causes and efficacy of mechanical ventilation were retrospectively analysed. (Results) Postoperative pneumonia was the cause of acute respiratory failure in 53 cases and ARDS caused by severe abdominal infection and severe acute pancreatitis in 38 cases. Of the 91 cases, complicated with COPD in 38 cases, severe malnutrion 32 cases, and hypokalemia 14 cases. Respiratory failure occurred at(4.08?2.45)days after operation. The duration of mechanical ventilation was(21.66?21.42)days; 33 cases died, and 58 cases were successfully recovered with mechanical ventilation.Conclusions The (management) of acute respiratory failure after abdominal asurgery should be rational use of mechanical (ventilation), adjustment of weaning strategy and avoidance of dependance on mechanical ventilation. Timely treatment of the primary disease, effective control of abdominal infection and aggressive symptomatic and (supportive) treatment are factors that affect the success or failure of mechanical ventilation.
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Objectives: To investigate the distribution of common pathogens and their antibiotic resistance from patiens with catheter related sepsis (CRS).Methods: Catheter bacteria cultrure and antibiotic sensitivity test were performed from 69 patiens with CRS.Results: The common pathogens in CRS were fungi (41.1%),Gram-positive cocci (35.6%)and Gram-negtive bacilli (23.3%). Non-C. albicans species were major pathogen (19/30 stranins).The most strains were staphylococcus epidermidis in Gram-positive cocci and the most of them were Methicillin resistant.No vancomycin resistant strains were found. The Gram negative bacilli were often resistant to third generation cephalosporens.Conclusions: The dorminant pathogens of CRS are fungi and gram positive cocci and we should pay more attention to pathogens of resistence to antibiotics. In order to control CRS, CVC must be used reasonably and shorten the duration of retention.