Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

Erythropoietin inhibits angiotensin Ⅱ induced cardiomyocyte hypertrophy in vitro via activating PI3K/Akt-eNOS pathway

Objective To explore the effect of erythropoietin (EPO) on angiotensin Ⅱ (Ang Ⅱ) induced neonatal rat cardiomyocyte hypertrophy and the association with PI3K/Akt-eNOS signaling pathway. Methods Cardiomyocytes were isolated from new-born Sprague-Dawley rats and stimulated by Ang Ⅱ in vitro. The cell surface area and mRNA expression of atrial natriuretic factor (ANF) of cardiomyocytes were determined in the presence and absence of various concentrations of EPO, phosphatidylinositol 3'-kinase (PI3K) inhibitor LY294002 and nitric oxide synthase (NOS) inhibitor L-NAME. Intracellular signal molecules, such as Akt, phosphorylated Akt, eNOS and phosphorylated eNOS protein expressions were detected by western blot. Nitric oxide (NO) level in the supernatant of cultured cardiomyocytes was assayed by NO assay kit. Results EPO (20 U/ml) significantly inhibited Ang Ⅱ induced cardiomyocyte hypertrophy as shown by decreased cell surface area and ANF mRNA expression (all P ＜0.05). EPO also activated Akt and enhanced the expression of eNOS and its phosphorylation (all P ＜ 0.05), increased the NO production (P ＜0.01). These effects could be partially abolished by cotreatment with LY294002 or L-NAME (all P ＜ 0.05). Conclusion EPO attenuates Ang Ⅱ induced cardiomyocytes hypertrophy via activating PI3K-Akt-eNOS pathway and promoting NO production.     

冠状动脉瘘的研究进展

冠状动脉瘘（coronary artery fistulas,CAF）是指心脏在胚胎发育过程中,心肌窦状间隙未能退化而持续存在所形成的冠状动脉主干或其分支与某个心腔或血管形成的异常通道,是一种十分少见的先天性心血管畸形。本文复习相关文献,对CAF的诊疗进展综述如下。     

长节段心肌桥合并慢血流引发心内膜下心肌梗死1例并文献复习

心肌桥是覆盖于冠状动脉上的浅层心肌,长节段的心肌桥对冠状动脉血流影响大,可出现心绞痛及心肌梗死,冠状动脉CT血管造影（CTA）及冠状动脉造影对其有较高诊断价值。慢血流指冠状动脉造影提示冠状动脉血流为TIMI 2级及以下,可导致心肌细胞水平低灌注,引起相应部位缺血。当心肌桥及慢血流同时存在时,则明显增加心血管事件发生率,造成严重后果,本文就两者并存而引发的1例心内膜下心肌梗死进行分析。     

经皮冠状动脉介入治疗右冠状动脉起源异常的不稳定型心绞痛

目的分析右冠状动脉（fight coronary artery,RCA）起源异常的不稳定型心绞痛经皮冠状动脉介入（percutaneous coronary intervention．PCI）治疗的临床特点。方法回顾性分析2005年10月至2012年10月武汉市第五人民医院收治行PCI治疗的不稳定型心绞痛合并RCA起源异常5例患者的临床资料。结果共计623例不稳定型心绞痛患者中6例合并存在RCA起源异常,其中5例罪犯血管为RCA,发生率0．96％。5例患者中男3例,女2例．中位年龄57（32～75）岁;其中RCA起源于左冠状窦3例,起源于嵴上1例,起源于主动脉前壁1例;单支血管病变4例,两支血管病变1例;4例植入药物洗脱支架1枚,1例植入药物洗脱支架2枚;5例PCI治疗围术期无夹层、血栓、心肌梗死、心力衰竭、脑卒中、死亡等并发症发生;随访14．6（6-24）个月,无心绞痛、死亡、再次冠状动脉事件入院、再次血管化等主要心血管事件发生。结论PCI治疗为RCA起源异常的不稳定型心绞痛患者提供了一种安全有效的治疗方法。     

糖尿病患者非高密度脂蛋白胆固醇和载脂蛋白A-Ⅰ比值与冠状动脉病变程度的相关性

目的探讨非HDL-C(NHDL-C)/载脂蛋白A-Ⅰ(apoA-Ⅰ)比值与2型糖尿病患者冠状动脉病变严重程度的相关性。方法选择因劳力性胸痛而行冠状动脉造影的2型糖尿病患者373例,依据Gensini评分三分位分为3组,低分组<8分(143例);中分组8²8分(109例);高分组>28分(121例),评价NHDL-C/apoA-Ⅰ比值与冠状动脉病变严重程度的相关性。结果 3组患者HDL-C、脂蛋白(a)、apoB、NHDL-C、NHDL-C/apoA-Ⅰ比值等比较,差异有统计学意义(P<0.05,P<0.01);Pearson相关分析和Spearman相关分析均显示,2型糖尿病患者NHDL-C/apo-A-Ⅰ比值与Gensini评分呈正相关(r=0.146,P<0.01;r=0.127,P<0.05)。多元线性回归分析显示,2型糖尿病患者NHDL-C/apoA-Ⅰ比值与冠状动脉病变严重程度独立相关(偏相关回归系数=3.361,P<0.05)。结论 NHDL-C/apoA-Ⅰ与2型糖尿病患者冠状动脉病变严重程度独立相关。     

血栓抽吸导管在ACS急诊PCI中的临床应用研究

目的探讨血栓抽吸导管治疗在ACS常规急诊PCI中的临床疗效。方法选择2010年1月-2011年5月我院住院行急诊经皮冠状动脉介入（PCI）治疗的93例急性ST段抬高型心肌梗死和高危、极高危非ST段抬高急性冠脉综合症（ACS）患者,随机分为联用ThrombusterⅡ血栓抽吸导管治疗为A组（51例）,同期未应用血栓抽吸导管治疗为B组（42例）。比较两组患者术后心肌梗死溶栓（TIMI）血流、校正TIMI帧数（CTFC）、术后心肌呈色分级（BMG）、术后ST段抬高回落幅度及左心室射血分数（LVEF）、住院期间主要心血管不良事件（MACE）有无差异。结果 A组TIMI血流3级、CTFC、BMG、术后ST段抬高回落幅度及LVEF均优于B组,差异均有统计学意义（P〈0.05）。两组患者院内MACE发生率比较,差异无统计学意义（P〉0.05）。结论在ACS常规急诊PCI中联用ThrombusterⅡ血栓抽吸导管治疗可显著改善患者TIMI血流、心肌组织水平灌注及术后心功能,但住院期间MACE的发生率无差异。     

罗汉果皂苷对阿霉素心肌损伤大鼠氧化应激和凋亡调节作用研究

目的 :从氧化应激和凋亡途径研究罗汉果皂苷对阿霉素心肌损伤大鼠的治疗作用,以为罗汉果皂苷治疗阿霉素心肌损伤提供基础实验理论。方法 :60只清洁级雄性SD大鼠采用一次性尾静脉注射阿霉素18 mg/kg构建阿霉素心肌损伤模型,模型构建成功后按照随机数字法将其分为正常组,模型组以及罗汉果皂苷低、中和高剂量治疗组,每组12只,罗汉果皂苷治疗4周后,收集血清和心脏,检测心肌病理学、心功能、血清SOD和MDA,同时采用Western Blotting和实时荧光定量检测心肌组织中Bax、Bcl-2蛋白和mRNA的表达特点。结果 :HE染色可见正常组心肌纤维排列整齐,模型组则有明显的心肌排列紊乱,与模型组相比,罗汉果皂苷低、中和高剂量有不同程度的减轻;与正常组相比,模型组AST、LDH、CK-MB和MDA明显升高(P0.05),罗汉果皂苷3个剂量组均可以明显降低上述几个指标(P0.05);与正常组相比,模型组SOD明显降低(P0.05),罗汉果皂苷3个剂量组相较于模型组则明显升高(P0.05);与正常组相比,模型组Bax蛋白和mRNA明显升高(P0.05),Bcl-2蛋白和mRNA明显降低(P0.05),与模型组相比,罗汉果皂苷3个剂量组均可以降低Bax(P0.05),同时升高Bcl-2表达(P0.05)。结论 :罗汉果皂苷可增强阿霉素心肌损伤大鼠抗氧化能力,抑制心肌细胞凋亡,进而改善心功能。