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1.
Objective: To investigate the directed transplantation of allograftic bone marrow-derived mesenchymal stem cells (MSCs) in myocardial infarcted (MI) model rabbits. Materials and Methods: Rabbits were divided into 3 groups, heart infarcted model with MSCs transplanted treatment (MSCs group, n=12), heart infarcted model with PBS injection (control group, n=20), sham operation with PBS injection (sham group, n=l 7). MSCs labelled by BrdUrd were injected into the MI area of the MSCs group. The same volume of PBS was injected into the MI area of the control group and sham group. The mortality, LVIDd, LVIDs and LVEF Of the two groups were compared 4 weeks later. Tropomyosin inhibitory component (Tn I) and BrdUrd immunohistochemistry identified the engrafted cells 4 weeks after transplantation. Result: The mortality of the MSCs group was 16.7% (2/12), and remarkably lower than the control group's mortality [35% (7/20) (P<0.05)].Among the animals that survived for 4 weeks, the LVIDd and LVIDs of the MSCs group after operation were 1.17±0.21 cm and 0.74±0.13 cm, and remarkably lower than those of the model group, which were 1.64±0.14 cm and 1.19±0.12 cm (P<0.05); the LVEF of the MSCs group after operation was 63±6%, and remarkably higher than that of the model group,which was 53±6% (P<0.05). Among the 10 cases of animals that survived for 4 weeks in the MSCs group, in 8 cases (80%),the transplanted cells survived in the non MI, MI region and its periphery, and even farther away; part of them differentiated into cardiomyocytes; in 7 cases (70%), the transplanted cells participated in the formation of blood vessel tissue in the MI region. Conclusion: Transplanted allograftic MSCs can survive and differentiate into cardiomyocytes, form the blood vessels in the MI region. MSCs transplantation could improve the heart function after MI.  相似文献   
2.
目的:临床试验表明,Ⅰ类抗心律失常药物虽能抑制心肌梗塞病人的室性心律失常,但增加死亡率,而胺碘酮(Ⅲ类药物)可提高心肌缺血患者的生存率.心室中层肌细胞(M细胞)有其独特的电生理特性并在心律失常发生中起重要作用.方法:采用细胞内玻璃微电极技术,用含胺碘硐或心律平的模拟缺血液灌流M细胞,了解在缺血情况下,两种药物分别对M细胞电生理有何影响.结果:(1)犬左心室M细胞的动作电位呈现出与心外膜层肌细胞相似的峰-谷-穹窿(spike and dome)形态;动作电位时程(APD)随基础起搏周长(BCL)延长而明显延长,即频率依赖性.(2)模拟缺血使M细胞的静息电位(RP)除极、动作电位幅值(APA)和Vmax减小、APD缩短,其APD的频率依赖性减弱或消失.(3)胺碘硐可延缓或减轻缺血引起的电生理变化.(4)心律平明显抑制M细胞的Vmax、APA,并随频率加快而作用增强.进一步加重了缺血引起的动作电位参数的改变,并可造成传导延缓或阻滞.结论:胺碘酮可减轻而心律平则加重缺血引起的M细胞的电生理改变.部分地解释了上述临床试验的结果.  相似文献   
3.
目的 探讨血浆可溶性血栓调节蛋白(Soluble thrombmodulin,sTM)与脑梗塞和脑出血患者小血管损伤、动脉粥样硬化的关系。方法 应用酶联免疫吸附方法(Enzyme-Linked Immunosorbent Assays,ELISA),检测60例脑梗塞患者、56例脑出血患者和64例健康对照的sTM水平,并分析sTM与血脂、血压的关系。结果 脑梗塞和脑出血的甘油三脂、舒张期血压明显高于对照组;脑梗塞和脑出血的高密度脂蛋白显著低于对照组;脑出血组的收缩期血压明显高于其他两组;脑梗塞的 胆固醇水平显著高于其他两组;脑出血的sTM显著高于脑梗塞和对照组,而脑梗塞的sTM显著高于对照组。sTM与总胆固醇、甘油三脂、收缩和舒张期血压水平显著正相关;sTM与高密度脂蛋白水平成显著负相关。结论 脑梗塞和脑出血存在由高血压和动脉粥样硬化导致的小血管损伤。sTM是脑卒中的独立危险因子。  相似文献   
4.
Cell therapy in congestive heart failure   总被引:5,自引:0,他引:5  
Congestive heart failure (CHF) has emerged as a major worldwide epidemic and its main causes seem to be the aging of the population and the survival of patients with post-myocardial infarction. Cardiomyocyte dropout (necrosis and apoptosis) plays a critical role in the progress of CHF; thus treatment of CHF by exogenous cell implantation will be a promising medical approach. In the acute phase of cardiac damage cardiac stem cells (CSCs) within the heart divide symmetrically and/or asymmetrically in response to the change of heart homeostasis, and at the same time homing of bone marrow stem cells (BMCs) to injured area is thought to occur, which not only reconstitutes CSC population to normal levels but also repairs the heart by differentiation into cardiac tissue. So far, basic studies by using potential sources such as BMCs and CSCs to treat animat CHF have shown improved ventricular remodelling and heart function. Recently, however, a few of randomized, double-blind, placebo-controlled clinical trials demonstrated mixed results in heart failure with BMC therapy during acute myocardial infarction.  相似文献   
5.
Objective: The beneficial effect of percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI) has been well established, but there is the problem of no-reflow phenomenon which is an adverse prognostic factor in primary PCI. In the present study the effect of a distal protection device (PercuSurge GuardWire; GW) on epicardial blood flow and myocardial perfusion was evaluated. Methods and Results: Patients with AMI were randomly divided into 2 groups, the GW and the control groups. The GW group included 52 patients with AMI who underwent primary PCI with GW protection and the control group included 60 patients who underwent primary PCI without GW protection. Epicardial blood flow in the infarct-related artery (IRA) and myocardial perfusion were evaluated according to the thrombolysis in myocardial infarction (TIMI) flow grade and the myocardial blush grade (MBG). We found TIMI score of 3 was obtained significantly more frequently in the GW group (96%) than in the control group (80%). The MBG score of 3 was obtained also significantly greater in the GW group (65%) than in the control group (33%). Conclusion: Primary PCI with GW protection can significantly improve epicardial blood flow and myocardial perfusion.  相似文献   
6.
摘要:目的:探讨抗阻训练对心肌梗死(myocardial infarction, MI)大鼠心脏和骨骼肌形态结构及神经调节蛋白1(Neuregulin1, NRG1)表征的影响及其性别差异。方法:3月龄Sprague Dawley大鼠,随机分为雄性假心梗组(MS)、雄性心梗安静组(MMI)、雄性心梗运动组(MMR)、雌性假心梗组(FS),雌性心梗安静组(FMI)和雌性心梗运动组(FMR),每组8只。MMR和FMR组进行为期4wk负荷渐进性递增抗阻训练。血流动力学测定心功能;组织学染色观察并计算形态学变化;检测心脏和骨骼肌中NRG1和ErbB2/4受体的表达变化。结果:MI后大鼠心功能显著降低,心肌组织出现替代性纤维化,腓肠肌质量和细胞横截面积不同程度减小。抗阻训练显著提高了MI大鼠心功能,增加了腓肠肌相对质量和细胞横截面积,同时显著上调雄性MI大鼠心肌和骨骼肌中NRG1蛋白水平及雄性和雌性MI大鼠ErbB2和ErbB4的表达(p<0.05, p<0.01)。结论:抗阻训练促进MI大鼠心功能改善和骨骼肌生长,上调心肌和骨骼肌中NRG1及其受体表达,且不同性别之间存在程度差异性。  相似文献   
7.
To study the protective role of Arogh on isoproterenol induced myocardial damage in rats. The effect of Arogh pretreatment on isoproterenol induced myocardial damage was assessed by studying the levels of lipid peroxides and changes in the activity of marker enzymes such as creatine kinase, lactate dehydrogenase and transaminases in serum and heart tissue. In isoproterenol administered rats, a significant decrease was observed in the activity of marker enzymes in the heart with a corresponding increase in their levels in serum. Lipid peroxide levels increased significantly in the serum and heart. In rats pretreated with arogh, the level of lipid peroxides and the activity of marker enzymes were maintained at near normal values. Pretreatment with Arogh offered a protective effect against isoproterenol induced myocardial damage in rats as evidenced by LDH isoenzyme patterm and histopathological studies of heart tissue.  相似文献   
8.
目的:探讨早期运动对脑梗死偏瘫患者肢体功能及生活能力的影响。方法:选择脑梗死偏瘫患者167例,随机为观察组(85例)和对照组(82例),2组均常规进行神经内科药物治疗,观察组加以运动疗法,分别于治疗前及治疗后1个月和3个月测评患者肢体运动功能(FMA)和日常生活活动能力(MBI,采用Barthel指数)。结果:2组治疗...  相似文献   
9.

Objective

To investigate stretch-induced electrophysiological changes in chronically infarcted hearts and the effect of streptomycin (SM) on these changes in vivo.

Methods

Sixty Wistar rats were divided randomly into four groups: a control group (n=15), an SM group (n=15), a myocardial infarction (MI) group (n=15), and an MI+SM group (n=15). Chronic MI was obtained by ligating the left anterior descending branch (LAD) of rat hearts for eight weeks. The in vivo blockade of stretch-activated ion channels (SACs) was achieved by intramuscular injection of SM (180 mg/(kg·d)) for seven days after operation. The hearts were stretched for 5 s by occlusion of the aortic arch. Suction electrodes were placed on the anterior wall of left ventricle to record the monophasic action potential (MAP). The effect of stretching was examined by assessing the 90% monophasic action potential duration (MAPD90), premature ventricular beats (PVBs), and ventricular tachycardia (VT).

Results

The MAPD90 decreased during stretching in both the control (from (50.27±5.61) ms to (46.27±4.51) ms, P<0.05) and MI groups (from (65.47±6.38) ms to (57.47±5.76 ms), P<0.01). SM inhibited the decrease in MAPD90 during inflation ((46.27±4.51) ms vs. (49.53±3.52) ms, P<0.05 in normal hearts; (57.47±5.76) ms vs. (61.87±5.33) ms, P<0.05 in MI hearts). The occurrence of PVBs and VT in the MI group increased compared with that in the control group (PVB: 7.93±1.66 vs. 1.80±0.86, P<0.01; VT: 7 vs. 1, P<0.05). SM decreased the occurrence of PVBs in both normal and MI hearts (0.93±0.59 vs. 1.80±0.86 in normal hearts, P<0.05; 5.40±1.18 vs. 7.93±1.66 in MI hearts, P<0.01).

Conclusions

Stretch-induced MAPD90 changes and arrhythmias were observed in chronically infarcted myocardium. The use of SM in vivo decreased the incidence of PVBs but not of VT. This suggests that SACs may be involved in mechanoelectric feedback (MEF), but that there might be other mechanisms involved in causing VT in chronic MI.  相似文献   
10.
To analyse the association of high sensitivity C-reactive (hsCRP) protein levels and −717A/G single nucleotide polymorphism of CRP with acute myocardial infarction (AMI) in the Indian population. Study population included 100 MI cases wherein 32 patients had experienced previous MI (MI-Group-1), 68 MI cases were recruited at presentation (MI-Group-2) and equal number of age and gender matched healthy individuals. hsCRP levels were determined by ELISA and genotyping of −717A/G was carried out by polymerase chain reaction-based restriction digestion method. The −717A/G genotypes did not influence hsCRP level and their distribution did not differ between groups. However, in the present study hsCRP demonstrated significant correlation with BMI in controls of both the genders and with triglycerides in females of AMI at presentation who otherwise are with low risk profile. Identifying traditional risk factors associated with inflammation may help in controlling the acute event.  相似文献   
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