多巴酚丁胺试验在心肌断层显像中的应用研究

采用多巴酚丁胺试验心肌断层显像的方法对14例可疑冠心病,8例心绞痛和3例心肌梗塞病人进行了检查。试验中发现,病人用药前后心率和血压的变化有显著性差异(P<0.01)。大部分受检者出现心悸、胸闷,少数病人有恶心、头痛,一般在停药后10分钟完全恢复正常,未发现严重副作用。结果表明,多巴酚丁胺试验效应近似运动生理变化,是一种安全有效的药物应激试验方法。结合心肌断层显像,对评价心肌缺血有较大临床意义。     

Estrogen receptor genotype modulates myocardial perfusion in young men

Most of the effects of estrogens are mediated by estrogen receptors. Vascular endothelial cells and smooth muscle cells express estrogen receptor (ESR1) in both genders. A long genotype group of a common thymine-adenine (TA) dinucleotide repeat polymorphism in the regulatory region of this gene has previously been related to coronary artery disease. The present study examined whether coronary blood flow is affected by this genotype. A total of 49 healthy men were genotyped by PCR and divided into three groups according to median number of the ESR1 promoter TA repeat (=19), i.e., in the short allele genotype group both alleles were of fewer than 19 repeats whereas in the long allele group both alleles were 19 repeats or more. The intermediate group comprised men who had one short and one long allele. Myocardial blood flow was measured by positron emission tomography using [¹⁵O]water, performed at rest and during adenosine stimulation. Men with long alleles had lower adenosine-stimulated coronary flow than those with short alleles and those with one short and one long allelle. Our results suggest that adenosine-stimulated myocardial perfusion is lower in subjects with ESR1 long alleles than the other TA repeat genotypes.     

辛伐他汀对大鼠心肌组织中低氧诱导因子1α表达的影响

目的：了解他汀类降脂药对低氧诱导因子1α（HIF1α）表达的影响,探讨其除降脂以外的抗心肌缺血作用机制。方法：将大鼠随机分为对照组、辛伐他汀组、心肌缺血组和辛伐他汀＋心肌缺血组。给辛伐他汀药4周后心肌缺血组和辛伐他汀＋心肌缺血组通过结扎冠状动脉左前降支致大鼠急性心肌缺血。分别用逆转录聚合酶链式反应(RT-PCR)法和Western blotting法及免疫组化法检测各组心肌组织中HIF1α mRNA 和蛋白的表达。结果：辛伐他汀和心肌缺血组均能使HIF1α表达明显高于对照组(P<0.01)，心肌缺血前辛伐他汀预处理可使HIF1α表达进一步增高(P<0.01)。结论：辛伐他汀可能是通过上调HIF1α表达促进新生血管形成，治疗心肌缺血。     

川芎嗪对急性心肌梗死血运重建后"心肌无复流"患者心肌组织灌注的影响

目的 观察川芎嗪对急性心肌梗死（AMI）患者梗死相关血管（mA）再通后心肌无复流（No．reflow，NR）现象的疗效。方法 首次急性sr段抬高心肌梗死（STEMI）患者，急诊经皮经腔冠状动脉介入（PCI）后，经单光子发射型计算机断层显像（SPECT）诊断为心肌NR者，随机分为治疗组（40例）和对照组（42例）。对照组接受常规治疗，治疗组在常规治疗基础上静脉给予川芎嗪注射液。分别于24h内（4—24h）及15d后（15—28d）复查SPECT，观察左室心肌灌注缺损积分（myocardium peffusion defect score，MPDS），左室射血分数（LVEF）、左室舒张末期容积（LVEDV）和左室收缩末期容积（LVESV）。结果 24h内及15d后，治疗组的MPDS均较PCI后即刻减低，其减低幅度均显著大于对照组（均P〈0．05）；两组的LVESV和LVEDV均呈增加趋势，但治疗组LVESV和LVEDV的增加幅度显著低于对照组（均P〈0．05）；15d后治疗组SPECT心肌NR的发生率显著低于对照组。结论 川芎嗪可显著改善心肌组织灌注，减轻心肌NR现象，从而缩小心肌坏死范围。抑制心室重构。     

热休克蛋白70对离体心脏心肌间质的保护作用

目的探讨热休克蛋白70（HSP70）对大鼠离体心脏心肌间质的影响。方法Wistar大鼠16只，分为2组：对照组（C，n=8），腹腔注射生理盐水0．4ml，24h后取离体心脏灌注HTK心脏保护液，4℃保存3h后建立Langendorff灌注模型，灌注KH液2h；实验组（E，n=8），腹腔注射重酒石酸去甲肾上腺素，24h后取离体心脏，方法同对照组。以心肌细胞中HSP70含量、血流动力学指标、心肌组织羟脯氨酸（HP）、内皮索（ET）含量和心肌超微结构等作为观察指标。结果HSP70含量E组与C组比较明显增高；E组心功能恢复方面优于C组（P〈0．05），HP含量优于C组（P〈0．01），ET含量低于C组（P〈0．01），心肌超微结构损伤较C组明显减轻。结论HSP 70对供心心肌间质具有保护作用。     

微小RNA-23b-3p通过靶向TGFBR3促进人心房肌成纤维细胞纤维化相关基因表达

目的:探究微小RNA-23b-3p(mi R-23b-3p)对人心房肌成纤维细胞中纤维化相关基因表达的作用及其可能作用靶基因。方法:分离并体外培养房颤患者心耳中原代心房肌成纤维细胞,并用细胞免疫荧光染色实验鉴定;双萤光素酶报告基因实验检测mi R-23b-3p与潜在靶基因转化生长因子β受体3(TGFBR3) 3'端非翻译区(3'-UTR)的结合作用; CCK-8、Ed U染色及Transwell实验检测细胞活力、增殖及迁移能力,RT-qPCR和Western blot法检测TGFBR3及纤维化相关基因的m RNA和蛋白表达。结果:在人心房肌成纤维细胞中过表达mi R-23b-3p不影响细胞的活力、增殖及迁移能力,但可显著增强细胞中纤维化相关基因COL1A1、COL3A1和ACTA2的表达(P 0. 05或P 0. 01)。双萤光素酶报告基因实验显示mi R-23b-3p与TGFBR3 3'-UTR有结合作用。RT-qPCR和Western blot结果证实mi R-23b-3p可在转录水平抑制TGFBR3表达。过表达mi R-23b-3p和沉默TGFBR3均能显著促进人心房肌成纤维细胞中Smad3激活和纤维化相关基因表达(P 0. 05或P 0. 01)。结论:TGFBR3是mi R-23b-3p的作用靶基因,并介导mi R-23b-3p促进心房肌成纤维细胞中纤维化相关基因表达。     

Decay-accelerating factor in the cardiomyocytes of normal individuals and patients with myocardial infarction

Summary The presence of decay-accelerating factor (DAF) was clearly demonstrated on the surface of normal cardiomyocytes. In patients who had died of myocardial infarction (MI) cardiomyocytes displayed different appearances: outside the ischaemically damaged region the myocytes showed no significant variations in DAF expression when compared with controls without MI. Within myocardial zones damaged by ischaemia, however, apparently normal myocytes showed large gaps in surface staining of DAF or formed clusters which were entirely devoid of reactivity with anti-DAF antibodies. The number of DAF-deficient myocytes increased with the extent of necrosis and also with the number of days between onset of MI and death. Even though injury to myocytes is to a large extent related to anoxia and to the presence of free oxygen radicals, the complement system also appears to be involved; DAF may have protective functions against complement-mediated injury. We speculate that phospholipase may be involved in the removal of DAF from the cardiomyocyte surface.This work was supported in part by grant no. 3.157.88 from the Swiss National Foundation for Scientific Research and a contribution from Sandoz Ltd. Pharma Division, Basel     

大鼠心肌匀浆上清液对骨髓间质干细胞诱导分化的影响

目的：探讨心肌匀浆上清液对大鼠骨髓间质干细胞（MSCs）诱导分化的影响。 方法： 体外分离培养大鼠MSCs，检测纯度。于原代培养第3 d加入自体心肌匀浆上清液持续作用1周。3周后，观察细胞形态，采用免疫细胞化学检测肌球蛋白重链和心肌特异性肌钙蛋白-T，RT-PCR方法检测Nkx2.5、α-MHC和ANP基因的表达。 结果： 大鼠MSCs经诱导后，表达肌球蛋白重链、心肌特异性肌钙蛋白-T和Nkx2.5、α-MHC基因，但未表达ANP基因，也未观察到肌管和闰盘样结构。 结论： 心肌匀浆上清液对MSCs具有定向诱导分化作用，但诱导不完全，具体机制仍需深入研究。     

Effect of adaptation to anoxia on antioxidative enzyme activity in the liver of stressed animals

All-Union Cardiologic Scientific Center, Academy of Medical Sciences of the USSR. Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Grenburg Medical Institute. (Presented by Academician of the Academy of Medical Sciences of the USSR I. K. Shkhvatsabaya.) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 106, No. 11, pp. 528–529, November, 1988.     

miR-30a-3p靶向NOD1对心肌细胞缺氧复氧损伤的影响

目的　探究miR-30a-3p与NOD1的靶向关系，及其对心肌细胞缺氧复氧损伤的影响和机制。 方法　将细胞分为Ctrl组、H/R组、miR-30a-3p mimic组和miR-30a-3p inhibitor组，经过缺氧复氧处理后，转染相应的miRNA处理细胞，RT-PCR检测miR-30a-3p和NOD1基因表达水平，荧光素酶报告检测miR-30a-3p和NOD1靶向关系，Western blot检测NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平，CCK8法检测细胞活性，Hoechst检测细胞凋亡，试剂盒检测LDH、CK、MDA、T-SOD水平。 结果　miR-30a-3p表达水平随缺氧复氧处理时间增长而下降，NOD1基因表达水平随缺氧复氧处理时间增长而升高。在荧光素酶报告实验中，NOD1 WT+miR-30a-3p mimic荧光素酶活性显著低于NOD1 WT+NC组。与Ctrl组比较，H/R组miR-30a-3p基因表达水平、细胞活性、T-SOD水平降低，NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平、LDH、CK、MDA水平、细胞凋亡率升高；与H/R组比较，miR-30a-3p mimic组miR-30a-3p基因表达水平、细胞活性、T-SOD水平升高，NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平、LDH、CK、MDA水平、细胞凋亡率降低，miR-30a-3p inhibitor组miR-30a-3p基因表达水平、细胞活性、T-SOD水平降低，NOD1、p-RPI2、p38 MAPK、NF-κB（p65）、cl-caspase-3蛋白表达水平、LDH、CK、MDA水平、细胞凋亡率升高。 结论　miR-30a-3p可靶向作用于NOD1，缓解心肌细胞缺氧复氧造成的损伤，其作用机制可能与调控NF-κB信号通路有关。