糖尿病对射血分数保留心力衰竭患者血生化指标、心脏指标及生活质量的影响

摘要 目的：探讨糖尿病（DM）对射血分数保留心力衰竭（HFpEF）患者血生化指标、心脏指标及生活质量的影响。方法：选取2017年1月-2019年5月我院收治的246例HFpEF患者作为研究对象,根据是否并发DM分为DM-HFpEF组（n=98）和NDM-HFpEF组（n=148）,比较两组患者基线资料、血生化指标,采用超声心动图检测心功能参数,采用明尼苏达心力衰竭生活质量调查表（MLHFQ）评价患者的生活质量。结果：两组患者体重、收缩压、合并冠心病比例、合并高血压比例相比较,差异有统计学意义（P＜0.05);与NDM-HFpEF组患者相比,DM-HFpEF组患者白细胞计数（WBC）、中性粒细胞计数（N）、血肌酐（Scr）、甘油三酯（TG）、空腹血糖（FBG）、餐后两小时血糖（2hPBG）、K⁺水平升高,血红蛋白（Hb）、高密度脂蛋白胆固醇（HDL-C）水平降低（P＜0.05);DM- HFpEF组舒张末期左心室容积指数（LVEDVI）低于NDM-HFpEF组患者,室间隔厚度(IVS)、左心室后壁厚度（PWTD）、E峰、E/e''高于NDM-HFpEF组患者,差异有统计学意义（P＜0.05);DM- HFpEF组患者MLHFQ中体力限制、社会限制、情绪、经济维度评分及总分高于NDM-HFpEF组患者,差异有统计学意义（P＜0.05)。结论：DM促进了HFpEF患者IVS、PWTD的增厚,降低了心脏舒张功能和患者的生活质量,且明显加重了HFpEF患者血糖血脂的代谢紊乱。     

Hey基因在心血管发育中的作用

人类的 H ey 基 因 编码 与果 蝇 hairy、 E nhancer-of-split相 似 的螺 旋 -环 -螺旋 亚 家族 转录 因 子 .到目 前为 止,N otch 信 号 途径 中已 明 确的 靶 基因 还不 多,它 们 就是 其中 的一 类 .因 此 ,它 们 是与 发 育过 程有 关的 基 因,这 些过 程 包括 横 向抑 制、组 织诱 导等 .人类 的遗 传 性突 变例 如 皮层 下梗 塞 的大 脑常 染 色体 显性 动 脉病 、A lag-ille 综合 症以 及小 鼠 模型 ,都 显示 出 N otch 信 号在 心 血管 发育 与 维持 过程 中 起着 重 要的 作用 .以 小 鼠和 斑马 鱼为 模型 进 行的 实 验也 表明 ,在 心 血管 形 成过 程中 ,H ey 基 因 在这 两个 物种 中 的同 源 基因 是 N otch 信 号中 最明 显的 转换 因 子 .     

KCTDIO is critical for heart and blood vessel development of zebrafish

KCTD10 is a member of the PDIP1 family, which is highly conserved during evolution, sharing a lot of similarities among human, mouse, and zebrafish. Recently, zebrafish KCTD13 has been identified to play an important role in the early development of brain and autism. However, the specific function of KCTD10 remains to be elucidated. In this study, experiments were carried out to determine the expression pattern of zebrafish KCTD10 mRNA during em- bryonic development. It was found that KCTD10 is a ma- ternal gene and KCTD10 is of great importance in the shaping of heart and blood vessels. Our data provide direct clues that knockdown of KCTDIO resulted in severe pericardial edema and loss of heart formation indicated by morphological observation and crucial heart markers like amhc, vmhc, and cmlc2. The heart defect caused by KCTD10 is linked to RhoA and PCNA. Flk-1 staining revealed that intersomitic vessels were lost in the trunk, although angioblasts could migrate to the midline. These findings could be helpful to better understand the determinants responsible for the heart and blood vessel defects.     

SFRP分子对心脏发育的影响

Wnt信号通路对心脏发育起着重要的作用.分泌型卷曲相关蛋白（SFRP）家族作为调控 Wnt信号的重要分子,对心脏发育和心肌分化的作用也越来越被人们所重视.最近,研究人员们对SFRP家族蛋白有了新的认识,认为它们不仅具有拮抗Wnt的作用,还对Wnt信号的转导有着复杂的调节作用.本文就SFRP分子与Wnt信号转导对心脏发育的影响进行综述.     

经颈静脉途径制备Beagle犬心脏记忆模型

目的经颈静脉途径应用心室起搏的方法制备心脏记忆犬模型。方法 8只普通级成年健康Beagle犬经腹腔麻醉后,Seldinger’s法穿刺颈外静脉成功后送入心内膜起搏电极,将电极头端固定于右室心尖部,近端连接于脉冲发生器。起搏频率设置较犬窦性心律时的基础心率快15%,保证起搏器连续起搏。结果连续起搏1周后所有动物均成功制备为心脏记忆模型。建模后犬的心率、呼吸、体重与建模前比较,无明显改变;所有模型组犬起搏前心电图均为窦性心律,起搏1周后出现心脏T波记忆,在下壁导联以及胸前导联均出现T波倒置,停止起搏后,心脏T波记忆逐渐消失;模型组犬与正常组犬心肌病理相比,无明显改变。结论经颈静脉途径应用心室起搏法建立心脏记忆犬模型的方法,具有手术简单,创伤小,诱发方式与临床相似等优点,为深入展开心脏记忆的机制研究奠定基础。     

人心脏型脂肪酸结合蛋白快速检测试剂盒的临床验证性研究

目的评价H-FABP快速检测试剂盒对急性心肌梗死(AMI)的早期诊断效果。方法比较H-FABP、CK、CK-MB和cTnT四种心肌标志物在AMI发作后6 h内的敏感性、准确性和时效性;比较H-FABP快速检测试剂盒对AMI患者和非AMI患者诊断的特异性。结果 H-FABP快速检测试剂盒的检测结果与临床诊断结果符合率为100%;在AMI发作后6 h内,H-FABP的敏感性和准确性优于CK、CK-MB,与cTnT相当。8例肾衰竭患者100%显示阳性,心源性疾病中主动脉关闭不全有1例(2.44%),房间隔缺损有2例(4.88%)显示阳性。结论 AMI发作后6 h内,H-FABP快速检测试剂盒对其具有较好的诊断价值。     

急性心肌梗死患者心电图碎裂QRS波与左心室收缩功能、心率变异性及心脏事件的关系研究

目的:探讨急性心肌梗死患者心电图碎裂QRS(f QRS)波与左心室收缩功能、心率变异性及心脏事件的关系。方法:收集2018年1月～2020年1月期间于本院进行治疗的急性心肌梗死患者124例,对患者行心电图检查,根据患者心电图是否出现f QRS波分成f QRS组(59例)和无f QRS组(65例),采用多普勒超声诊断仪对两组患者的左心室收缩功能进行检测对比,并对两组患者进行24h动态心电图检查,对两组患者的心率变异性指标进行统计对比。对两组患者进行为期3个月的随访观察,统计对比两组患者随访期间心脏事件的发生率。结果:f QRS组患者的左室射血分数(LVEF)低于无f QRS组,左心室舒张末期容积(LVEDV)、左心室舒张末期内径(LVEDD)均高于无f QRS组(P0.05)。f QRS组患者总标准差(SDNN)、两个相邻RR间期互差(PNN50)、差值均方根(RMSSD)均低于无f QRS组(P0.05)。随访期间f QRS组患者的心脏事件发生率为35.59%(21/59),高于无f QRS组患者的13.85%(9/65)(P0.05)。结论:伴有心电图f QRS波急性心肌梗死患者的左心室收缩功能降低,心率变异性指标降低,且心脏不良事件发生率增加,心电图f QRS波在一定程度上可作为急性心肌梗死患者心功能、心率变异性及心脏事件发生的监测手段。     

一种新的体外细胞牵张刺激装置

体外细胞机械刺激装置是研究细胞对机械牵张反应的一种研究设备。目前此类装置有多种,但是这些装置都存在一些不便之处。本文以商品化的Flexercell Strain Unit刺激装置为参照,设计一套离心力牵张装置。通过使贴壁细胞生长的培养板以一定的速度旋转,从而使心肌细胞受到固定大小的离心力的牵张作用。酶解分离3～5d SD大鼠心肌细胞,并分别给予12和24h机械刺激:传统的20%牵张刺激和180r/min的离心力刺激。以~3H-亮氨酸掺入量反映细胞的肥大指标,并测定牵张引起的血管紧张素Ⅱ的自分泌。同对照组相比,~3H-亮氨酸掺入在离心力牵张组显著升高[(1295.17±51.19)vs(1122.67± 51.63)in 12h;(1447.5±35.96)vs(1210.67±90.92)in 24h,P<0.05]。AngⅡ在离心力牵张组均比同期末牵张组均明显升高,12h为128%(P<0.05)和24h为139%(P<0.01)。经24h的牵张,培养液中乳酸脱氢酶活性在膜牵张组显著高于离心力牵张组[(14.5±8.7)U/Lvs (7.8±4.3)U/L,P<0.05]。新型改进的机械牵张装置能够有效刺激心肌细胞蛋白合成增加和AngⅡ的分泌增加,与FlexercellStrain Unit相比,离心力牵张装置对细胞的损害较轻微。     

Characterization of MR-1, a novel myofibrillogenesis regulator in human muscle

Myofibrils are components of both cardiac and skeletalmuscle cells. Myofibrillogenesis is a highly complexprocess that involves the expression and assembly ofmuscle proteins into sarcomeres [1]. The key componentsof sarcomeres are two filamentary proteins, actin andmyosin. Sarcomeric myosin is the molecular motor thattransduces energy from the hydrolysis of ATP into directedmovement and drives sarcomere shortening and musclecontraction. Each myosin hexamer is composed of twoheavy chains, two…     

Mechanical stretch induces mitochondria-dependent apoptosis in neonatal rat cardiomyocytes and G2／M accumulation in cardiac fibroblasts

Heart remodeling is associated with the loss of cardiomyocytes and increase of fibrous tissue owing to abnormal mechanical load in a number of heart disease conditions. In present study, a well-described in vitro sustained stretch model was employed to study mechanical stretch-induced responses in both neonatal cardiomyocytes and cardiac fibroblasts. Cardiomyocytes, but not cardiac fibroblasts, underwent mitochondria-dependent apoptosis as evidenced by cytochrome c (cyto c) and Smac/DIABLO release from mitochondria into cytosol accompanied by mitochondrial membrane potential (△ψm) reduction, indicative of mitochondrial permeability transition pore (PTP)opening. Cyclosporin A, an inhibitor of PTP, inhibited stretch-induced cyto c release, △ψm reduction and apoptosis,suggesting an important role of mitochondrial PTP in stretch-induced apoptosis. The stretch also resulted in increased expression of the pro-apoptotic Bcl-2 family proteins, including Bax and Bad, in cardiomyocytes, but not in fibroblasts. Bax was accumulated in mitochondria following stretch. Cell permeable Bid-BH3 peptide could induce and facilitate stretch-induced apoptosis and △ψm reduction in cardiomyocytes. These results suggest that Bcl-2 family proteins play an important role in coupling stretch signaling to mitochondrial death machinery, probably by targeting to PTP. Interestingly, the levels of p53 were increased at 12 h after stretch although we observed that Bax upregulation and apoptosis occurred as early as 1 h. Adenovirus delivered dominant negative p53 blocked Bax upregulation in cardiomyocytes but showed partial effect on preventing stretch-induced apoptosis, suggesting that p53 was only partially involved in mediating stretch-induced apoptosis. Furthermore, we showed that p21 was upregulated and cyclin B 1 was downregulated only in cardiac fibroblasts, which may be associated with G2/M accumulation in response to mechanical stretch.