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.
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, 1×103(group 1), 1×105(group 2), and 1×107(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,Pgt;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,Plt;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＝0015) 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.
目的:探讨动态心电图对无症状心肌缺血的诊断价值。方法:对138例冠心病(CHD)患者行24 h动态心电图检测。结果:共检出缺血型ST-T改变102例、723阵次。其中,无症状性心肌缺血562阵次(77.7%),发作时间高峰在6:00～11:00。结论:动态心电图是检测无症状心肌缺血的重要方法,对其病情的判断及早期防治具有重要的意义。
【摘要】目的探讨丹酚酸(Sal)B 配伍丹皮酚对大鼠心肌缺血再灌注损伤(MIRI)的保护作用。方法大鼠心肌缺血60 min 后再灌注90 min 造成大鼠心肌缺血再灌注损伤模型,测定给药后心肌组织匀浆、血浆中内皮素(ET)、血清中一氧化氮(NO)和一氧化氮合酶(NOS)的变化,并通过病理组织学检查,观察Sal B 配伍丹皮酚5、10、15 mg/kg对大鼠MIRI不同浓度和不同给药方法的治疗作用。结果Sa1 B配伍丹皮酚,中、高剂量组均能减少心肌组织和血浆中ET 的含量,提高NOS 的活性,增加NO的释放(Plt;005)。结论Sal B减轻大鼠MIRI 可能是通过调节ET/NO 系统的平衡,维持冠脉血管张力,改善心肌能量代谢障碍实现的。
ObjectiveTo compare the myocardial protective effect of HTK solution and St.ThomasⅡ(STH) solution in immature rabbit myocardium at different cardiac arrest time. MethodsAccording to cardioplegia and cardiac arrest time, 32 immature New Zealand white rabbits (aged 2-3 weeks) were randomly divided into four groups. A group SO (8 rabbits) underwent 1 hour cardiac arrest with STH solution, a group ST (8 rabbits) underwent 2 hours cardiac arrest with STH solution, a group HO (8 rabbits) underwent 1 hour cardiac arrest with HTK solution, a group Ht (8 rabbits) underwent 2 hours cardiac arrest with HTK solution. Compare the myocardial protective effect of HTK and STH solution in immature myocardium at different cardiac arrest time. ResultsThe Langendorff models were successfully established in 30 cases (8 cases in the group SO and HO, 7 cases in the group ST and HT). There were no statistical differences in hemodynamics and myocardial enzyme (CK-MB, LDH) (P > 0.05), but HTK solution reduced the activity of nitric oxide synthase (NOS) and content of malonaldehyde (MDA) and NO, maintained high activity of superoxide dismutase (SOD) and Ca2+-ATPase (P < 0.05), performed more effective myocardial protection for immature myocardium. ConclusionHTK solution has more effective myocardial protection for immature myocardium than STH solution does, but STH solution still has good outcomes within short cardiac arrest time (1h).
ObjectiveTo investigate whether emulsified isoflurane applied after an ischemic episode induces postconditioning in an ischemia model of myocardial injury and its underlying mechanism. MethodsBetween March and October 2012, using a model of in situ myocardial ischemia and reperfusion injury in rats, cardioprotective effects of emulsified isoflurane were examined by determining infarct size, myocardial damage markers and the concentration of tumor necrosis factor (TNF)-α. ResultsEmulsified isoflurane postconditioning limited infarct size compared with control groups. It increased serum concentrations of superoxide dismutase while decreased malonaldehyde. TNF-α positive cells were also significantly reduced in emulsified isoflurane group compared with control group. Infusion of intralipid had no effect on infarct size or other variables. ConclusionIntravenous administration of emulsified isoflurane after reperfusion protects hearts against reperfusion injury, which may be mediated by the inhibition of cardiac damage markers and the concentration of TNF-α.
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 αminimum 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.
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.