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find Keyword "心肌缺血" 26 results
  • Changes of the Level of G Protein in Newborn Guinea-pig Myocardium Undergoing Global Ischemic Reperfusion

    ObjectiveTo study the changes of levels of α subunits of stimulatory (Gsα) and inhibitory guanine nucleotide binding protein (Giα) in newborn guinea pig (0 2 days old) myocardium undergoing global ischemic reperfusion, and influences on the changes by St.Thomas Ⅱ and cold blood cardioplegic solution.MethodsThirty newborn guinea pigs were randomly assigned to three groups. GroupⅠ ( n = 10): the newborn hearts suffered by hypothermic global ischemia; group Ⅱ( n =10): the newborn hearts arrested by St. Thomas Ⅱ , and group Ⅲ ( n = 10): the newborn hearts arrested by cold blood cardioplegic solution. Levels of Gsα and Giα were investigated with Western blot analysis.ResultsNo differences of levels of Gsα and Giα were found in three groups before ischemia ( P gt;0.05). The level of Gsα after ischemia was significantly decreased than before ischemia in groupⅠand group Ⅱ ( P lt; 0 01), whereas no pronounced changes in group Ⅲ ( P gt;0.05) were noted after ischemia. The level of Gsα in group Ⅲ was not significantly changed after reperfusion compared with before ischemia( P gt;0 05), and it was much higher than those in groupⅠand group Ⅱ ( P lt; 0 01). Level of Giα was found not markedly changed in group Ⅲ after reperfusion compared with that before ischemia, but was notable higher in groupⅠand group Ⅱ( P lt;0.01). ConclusionsSignificant decrease of level of Gsα, whereas marked increase of level of Giα are found in myocardium of newborn guinea pig undergoing hypothermic (20℃) ischemic reperfusion. No impact of St. Thomas Ⅱ on these changes is verified, but recovery to the level of Gsα and Giα before ischemia is achieved by cold blood cardioplegic solution after ischemia and reperfusion. Unbalance between Gsα and Giα is the one of the mechanisms of ischemic reperfusion injury for immature myocardium.

    Release date:2016-08-30 06:24 Export PDF Favorites Scan
  • Protective Effect and Regulation Mechanism of Oxaloacetate on Myocardial Ischemia Reperfusion Injury in Rats

    ObjectiveTo investigate the protective effect and the regulation mechanism of oxaloacetate (OAA) on myocardial ischemia reperfusion injury in rats. MethodsSixty rats, weight ranged from 200 to 250 grams, were randomly divided into 6 groups:a negative control group, a sham operation control group, a model control group, an OAA pretreatment myocardial ischemia-reperfusion model group (three subgroups:15 mg/kg, 60 mg/kg, 240 mg/kg). We established the model of myocardial ischemia reperfusion of rats and recorded the internal pressure of left ventricle (LVSP), the maximal rate of left ventricular pressure change (±dp/dtmax) and left ventricular end diastolic pressure (LVEDP). We restored reperfusion 180 minutes after ligating the left anterior descending coronary artery 30 minutes and determinated cardiac troponin Ⅰ (cTn-I), lactate dehydrogenase (LDH), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px). We took out heart tissues, stained it and calculated the infarcted size. We used the Western blot to detect the expression of NF-E2 related factor 2 (Nrf2), Kelch-like ECH-associated protein-1 (Keap1) and heme oxygenase-1 (HO-1). ResultsCompared with the sham operation group, heart function indexes in the negative control group had no significant difference (P>0.05). But in the model control group there was a decrease (P<0.05) And the serum levels of LDH, cTn-I, and myocardial infarcted size were significantly increased (P<0.01). Compared with the model control group, heart function indexes in the OAA pretreatment groups improved, the serum LDH, cTn-I activity, and infarct size decreased (P<0.05), SOD and GSH-Px activity increased (P<0.05). And these results were statistically different (P<0.01) in the high dose OAA pretreatment groups. Compared with the model control group, the expression of Keap1 in the OAA pretreatment group was down-regulated (P<0.001) while total Nrf2, nucleus Nrf2 and its downstream HO-1 was up-regulated (P<0.001), which suggested that OAA enhanced antioxidant capacity by (at least in part) Keap1-Nrf2 pathway, resulting in reducing myocardial damage and protecting myocardium after acute myocardial ischemia reperfusion injury. ConclusionOxaloacetate can provide protective effects on myocardial ischemia reperfusion injury through down-regulating the expression of Keap1 and up-regulating the expression of Nrf2 and its downstream peroxiredoxins to improve antioxidant capacity.

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  • Combination Transplantation of Bone Marrow Mesenchymal Stem Cells and Hepatocyte Growth Factor Gene in the Treatment of Chronic Ischemic Heart Disease in Pigs

    Abstract: Objective To investigate the effects of hepatocyte growth factor(HGF)gene transfected bone marrow mesenchymal stem cells (MSCs)transplantation in pigs with chronic ischemic heart disease. Methods MSCs were isolated from pig bone marrow by density gradient centrifugation and adherent cell culture, purified, and determined by cellsurface antigens(CD34, CD44, CD71, Ⅷ factor and desmin). MSCs were transfected by adenovirus expressing hepatocyte growth factor(AdHGF), and the influence of HGF on the biological characteristics of MSCs was tested. The pig model of chronic myocardial ischemia was established by placing Ameroid ring inside the left circumflex coronary artery via leftthoracotomy. A total of 40 pigs were randomly divided into 5 groups (n=8) and were injected 5×106/ml MSCs+ 4×109 pfu 200 μl AdHGF (MSCs+ AdHGF group), 4×109 pfu 200 μl AdHGF (AdHGF group), 5×106/ml MSCs 200 μl(MSCs group),4×109 pfu 200 μl AdNull (AdNull group)and 1 ml saline(control group) into the ischemic myocardiumrespectively. Echocardiogram, digital subtraction angiography (DSA) of coronary artery, single photon emission computed tomography(SPECT) myocardial perfusion imaging and cardiomyocyte apoptosis were examined after 4 weeks. Results Positive CD44 and CD71 and negative CD34, Ⅷ factorand desmin were detected in MSCs by flow cytometer. HGF had a b influence on stimulating the proliferation and differentiation of MSCs. Echocardiogram examination showed that left ventricular end-diastolic volume(LVEDV),left ventricular ejection fraction(LVEF),fractional shortening(FS)of MSCs+ AdHGF group were significantly increased after treatment (P< 0.05). DSA detection showed that ischemic neovascularization of MSCs+ AdHGF group was significantly higher than those of AdHGF group and MSCs group (P< 0.05). SPECT showed that the left ventricular myocardium of MSCs+ AdHGF group appeared thickened,myocardial perfusion was significantly improved and the myocardial motion was significantly increased (P< 0.05). Vascular density of MSCs+ AdHGF group was significantly higher than those of AdHGF group and MSCs group by HE stain of myocardium [(39.4±1.2)/ HPF vs. (36.5±1.4)/ HPF and(34.5±1.7)/ HPF,P< 0.05]. Cardiomyocyte apoptosis rate of MSCs+ AdHGF group was significantly lower than those of AdHGF group and MSCs group by TUNEL stain (P< 0.05). Conclusion Combination transplantation can promote the angiogenesis of chronic ischemic myocardium, inhibit cardiomyocyte apoptosis and improve heart function in pigs with chronic ischemic heart disease. The effect of HGF gene transfected MSCs transplantation is better than that of MSCs or HGF transplantation alone.

    Release date:2016-08-30 05:50 Export PDF Favorites Scan
  • The Advance of Bone Marrow Mononuclear Cell Transplantation in Treating Ischemia Heart Disease

    The bone marrow mononuclear cell(BMMNC) subset comprises mesenchymal stem cells, hematopoietic stem cells, endothelial progenitor cells. These cells can differentiate into cardiomyocytes, vascular endothelial cells and smooth muscle cells, and they can also release a wide array of cytokines that exert their effects on surrounding cells, including inducing neovascularization, preventing apoptosis of home cells and homing of endogenous systemic repairing cells. Many trials have been developed to evaluate the effect of bone marrow mononuclear cell transplantation in treating ischemia heart diseases in this country and others. Several routes have been used to deliver these cells to human myocardium or to the coronary circulation in these trials, such as intracoronary injection, intravenous infusion, direct injection into the ventricular wall, or transepicardial/transendocardial infusions,and the cells are constructed into fragmented cell sheets to improve cell retention, or some cytokines are used to enhance therapeutic effect. Although the results of the recent clinical trials in this area are rather conflicting, these therapeutic approaches seem to be promising forthe treatment of ischemic heart disease. In this review, many aspects of bone marrow mononuclear cell transplantation in myocardial infarction are summarized such as the mechanism, delivery routes, retaining of cells, homing, survival and future development, etc. 

    Release date:2016-08-30 06:06 Export PDF Favorites Scan
  • Experimental Study of Treatment of Acute Myocardial Ischemia Transplanted by Autologous Bone Mesenchymal Stem Cells

    Abstract: Objective To evaluate if cardiac function and myocardial perfusion in acute ischemia myocardial transplanted by autologous bone mesenchymal stem cells (MSC) can be improved. Methods Sixteen New Zealand rabbits were studied.The left anterior descending coronary artery under the first diagonally branch was ligated to result in acute myocardial ischemia models,the sixteen models were divided into two groups with randomed number table. Control group(n=8): 0.6ml αminimum essential medium was injected into myocardium; transplanted group (n=8): 0.6ml medium of autologous MSC marked with 5-bromium,2-deoxy-uridine (BrdU) was injected into myocardium. Echocardiography were erformed to measure left ventricular ejection fraction(LVEF),as well as the displacement and strain of apex segment of left ventricle pre-ichemia,beforeand 4 weeks after treatment; the target myocardial tissues were harvested 4 weeks after treatment,double immunohistochemistry staining of anti-BrdU and anti-troponin T(TnT) were used to evaluate the survival and differentiation of implanted MSC; immunohistochemistry staining of anti-CD146 endothelium factor were used to evaluate the density of capillary vessels in treated myocardium. Results Double immunohistochemistry staining showed that positive cells were found in transplanted group and not found in control group. Anti-CD146 immunohistochemistry staining showed density of capillary vessels of transplanted group was significantly more than that of control group(Plt;0.05) ; LVEF,displacement and strain of cardiac apex of transplanted group improved significantly more than those of control group(Plt;0.05). Conclusion Transplanted to acute myocardium ischemia models of rabbits, MSC can differentiate into myocardium-like cells in myocardial microenvironment,and improve global and part cardiac systolic function and then improving perfusion of ischemia myocardium.

    Release date:2016-08-30 06:15 Export PDF Favorites Scan
  • 雌二醇对兔心肌缺血再灌注损伤的保护作用

    目的 探讨17b-雌二醇(E2)对兔心肌缺血再灌注(I/R)损伤的保护作用。 方法 通过结扎冠状动脉左前降支建立兔在体心肌I/R损伤模型,将36只兔随机分为3组(每组12只),对照组:心肌缺血前静脉注入1ml乙醇;早期组:心肌缺血前注入10μg/kg E2;晚期组:再灌注前注入10μg/kg E2。化学发光法测定E2的浓度,检测血清超氧化物歧化酶(SOD)、丙二醛(MDA)、肌酸激酶同工酶(CK-MB)的变化,称重法测定心肌梗死范围,TUNEL法检测心肌细胞凋亡。 结果 与对照组比较,早期组和晚期组CKMB、MDA含量明显降低(Plt;0.05),SOD活性明显升高(Plt;0.05),心肌梗死范围及凋亡指数显著降低(Plt;0.05),但早期组和晚期组之间比较差异无统计学意义。 结论 E2对减轻心肌I/R损伤的作用是在再灌注过程中,这种作用可能是通过抗氧化、抗凋亡和减少心肌细胞坏死途径实现的。

    Release date:2016-08-30 06:16 Export PDF Favorites Scan
  • Dose-Dependent Relationship of Bone Marrow Mesenchymal Stem Cells Transplantation to Cardiomyogenesis for Functional Regenerative Recovery after Myocardial Infarction

    Objective To investigate the dose-dependent relationship of bone marrow mesenchymal stem cells(MSCs) transplantation in improving ischemic myocardial dysfunction? in a rat ischemic heart model. Methods Myocardial infarction was induced in 32 inbred F344 rats by acute ligation of the left anterior descending(LAD) coronary artery. One week after ligation, the ratswere randomized? into four equal groups, with eight rats in each group. Equal volume Iscove’s modified Dulbecco’s medium was injected in the control group, 1×103(group 1), 1×105(group 2), and 1×107(group 3) 5-bromodeoxyuridine (BrdU) labeled bone marrow MSCs were injected into the infarcted myocardium. Cardiac function was evaluated by ultrasound before the ligation of the LAD, before the transplantation and the 4th week after transplantation. The expressions of BrdU,Connexin43,Myosin heavy chain β(MHC), and smooth muscle actin α(α-SMA) were detected by immunofluorescence and immunohistochemistry at the 4th week after transplantation. The amount of functional vessels stained by α-SMA was counted simultaneously. Results At the 4th week? after transplantation, the ejection fraction(EF) in goup 2 was more significantly improved than that in group1(0.54±0.20 vs. 0.34±0.16, P=0.004) and EF in group 3 was more significantly improved than that in group 2(0.71±0.24 vs. 0.54±0.20,P=0.018), whereas no significant difference between group 1 and control group was detected (0.34±0.16 vs. 0.36±0.15,Pgt;0.05). The BrdU labeled MSCs could be found in host myocardium. The number of cells in group 2 by double staining both for BrdU and for MHC observed in ischemic myocardium were significantly more than that in group 1? (323.20±91.62 n/HP vs. 51.75±27.58 n/HP,P=0.049) and the same was true between group 3 and group 2(409.75±106.65 n/HP vs. 323.20±91.62 n/HP,Plt;0.001), whereas the result of control group was negative.The majority of transplanted cells were found positive staining both for MHC and for Connexin43 in all groups. There were lots of positive staining of α-SMA whose form were partly irregular in ischemic myocardium indicating that there was neovascularization in group1 and control group. More neovascularization in group2 was found than that in group 1 (28.38±12.79 n/HP vs. 22.75±9.07 n/HP, P=0015) and more neovascularization in group 3 was found? than that in group 2 (35.63±13.27 n/HP vs. 28.38±12.79 n/HP, P=0.002) . Conclusion Transplanted into infarcted myocardium, bone marrow MSCs may have significant and dose-dependent potential for cardiomyogenesis with functional recovery from myocardial ischemia.

    Release date:2016-08-30 06:16 Export PDF Favorites Scan
  • Emergency surgery on severe myocardium ischemia of early post-coronary artery bypass grafting

    Objective To summarize the experience of emergency coronary artery bypass grafting(CABG) on serious myocardium ischemia in early post CABG. Methods Between 1998 and 2002, emergency redo CABG was performed in 13 patients with serious early post operative myocardium ischemia. The causes included vein graft embolize(4 cases),uncompleted revascularize(3 cases), graft spasm(1 case) and anastomose stenosis or occlusion (5 cases). The grafts was 1 3(1.8±0.9) during redo CABG. Results There were 6 deaths, the mortality was 46%. The mean follow up was 31 months. There was no recurrence of angina. NYHA function was Ⅰ Ⅱ. Conclusion Emergency CABG is an important method in saving the patients with severe myocardium ischemia in early post CABG. The perioperative prevention and early treatment should be emphasized.

    Release date:2016-08-30 06:27 Export PDF Favorites Scan
  • 复制缺陷的重组腺病毒载体直接转染猪慢性缺血心肌的研究

    目的 建立猪慢性心肌缺血模型,评价腺病毒载体的转染效率和持续时间. 方法 应用磷酸钙沉淀法制备携带大肠杆菌LacZ基因复制缺陷的重组腺病毒(Ad.LacZ),将健康家猪8条随机分为实验组和对照组,每组4条.两组猪均经左前外侧开胸,于冠状动脉左回旋支(LCX)放置Ameroid环, 28天后二次开胸,实验组:在缺血心肌部位每点直接注射Ad.LacZ 100μl,1010噬斑形成单位,共10点;对照组:在缺血心肌部位每点注射磷酸盐缓冲液(PBS)100μl,共10点.于注射后3天、7天和28天对缺血心肌进行染色和病理观察. 结果 冠状动脉造影证实LCX完全闭塞,心肌有缺血和小面积心肌梗死;实验组注射Ad.LacZ后第3天、7天和28天X-gal染色有阳性细胞,以7天时明显,对照组无阳性细胞. 结论 应用Ameroid环可成功建立猪慢性心肌缺血模型,腺病毒载体转染缺血心肌基因表达可持续4周.

    Release date:2016-08-30 06:32 Export PDF Favorites Scan
  • 心肌缺血-再灌注中核因子-kB活性变化及其对中性粒细胞黏附的影响

    目的 研究心肌缺血-再灌注时中性粒细胞(PMN)内核因子-kB(NF-kB)活性变化与PMN细胞间黏附分子(ICAM-1)表达及其PMN黏附的关系. 方法 新西兰白兔24只,随机分为3组,每组8只.组1:结扎兔左冠状动脉前降支造成心肌缺血45分钟后再开放;组2:心肌缺血同组1,用吡咯基二硫氨基甲酸酯(PDTC)于心肌缺血前10分钟静脉注射(15mg/kg); 对照组:不作动脉结扎.3组分别于缺血前、再灌注30分钟、60分钟、90分钟、120分钟、240分钟和360分钟时用流式细胞仪检测PMN ICAM-1的表达,凝胶电泳迁移率分析检测NF-kB的活性,测定PMN与脐静脉内皮细胞黏附率(PMN-EC-340). 结果 组1中PMN ICAM-1的表达在心肌再灌注120分钟时开始升高,并与PMN-EC-340黏附率变化有显著的相关性;NF-kB 活性于心肌再灌注30分钟后开始增高,120分钟达高峰,之后活性逐渐下降. 组2中PMN ICAM-1、NF-kB活化程度和PMN-EC-340黏附率升高幅度均低于组1(P=0.041,0.029,0.034). 结论 心肌缺血-再灌注时刺激NF-kB的活化,启动PMN ICAM-1的表达而参与缺血-再灌注损伤的发生过程.

    Release date:2016-08-30 06:31 Export PDF Favorites Scan
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