涂层可降解药物洗脱支架"叠加"技术治疗右冠状动脉瘤1例

<正>1病例资料患者男性,80岁,因"发作性胸痛10余年,再发加重9 h"入院。患者10年前曾因"不稳定性心绞痛"行冠状动脉旁路移植术,术后严格实施冠心病二级预防药物治疗,无心绞痛发作。9 h前,患者再次频繁缺血性胸痛发作,口服硝酸甘油片等抗心绞痛药物无效而入院。既往有原发性高血压(高血压)病史20余年,规律服药治疗,血压控制尚可,否认糖尿病及风湿结缔组织疾病病史。入院体检:体温36.5℃,脉搏92bpm,呼吸20bpm,血压140/90 mmHg     

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。     

苦瓜总皂苷对慢性心衰大鼠Caspase-3和MMP-2表达影响

目的:探讨分析苦瓜总皂苷对慢性心衰大鼠心脏组织中Caspase-3和MMP-2表达的影响。方法:60只SD大鼠按照随机数字法分为正常组、模型组以及苦瓜总皂苷低、中和高剂量治疗组,每组12只,适应性喂养14d后给予注射盐酸去甲肾上腺素(ISO)构建心衰大鼠模型,模型建立成功后,苦瓜总皂苷低、中和高剂量组分别给予苦瓜总皂苷10、20和40 mg/(kg·d)皮下注射,注射时分散于500μL的生理盐水中,正常组和模型组则给予等量的生理盐水注射,8周后采用超声仪评价大鼠心功能指标,同时检测炎性因子TNF-α和IL-10含量,免疫组化、Western以及实时荧光定量PCR检测心肌组织中Caspase-3和MMP-2表达的特点。结果:在实验期内,模型组大鼠有明显精神萎靡,同时饮食量均降低,苦瓜总皂苷3个治疗组可明显改善上述症状,此外模型组有3只死亡,苦瓜总皂苷低、中和高剂量组分别死亡2只、2只和1只;与正常组相比,模型组LVDD和LVDS明显升高(P0.05),LVEF和LVFS明显降低(P0.05),与模型组相比,苦瓜总皂苷低剂量和中剂量组没有明显改善,而苦瓜总皂苷高剂量组LVDD和LVDS明显降低(P0.05),LVEF和LVFS则明显升高(P0.05);此外苦瓜总皂苷3个治疗组可以明显降低炎性因子TNF-α和IL-10的表达;与正常组相比,模型组Caspase-3和MMP-2表达明显升高(P0.05),与模型组相比,苦瓜总皂苷3个治疗组则可以明显降低其表达(P0.05)。结论:苦瓜总皂苷能够有效改善ISO所致的慢性心衰大鼠心功能,降低炎症反应,其机理可能与其可以抑制心脏组织中Caspase-3和MMP-2的表达有关。     

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.     

血清肾素-血管紧张素醛固酮水平与代谢综合征的相关性

目的:研究血清肾素-血管紧张素醛固酮水平与代谢综合征(MS)及其组分的相关性。方法:198例体检者采空腹静脉血查血糖(FPG)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)、总胆固醇(TC)及肾素、血管紧张素、醛固酮水平、行糖耐量(OGTT)检测,测血压、身高及体重,计算体重指数(BMI)及醛固酮肾素比值,相关回归分析血清RAAS水平与血脂、血压、血糖、BMI及MS的相关性。根据是否患有MS分为MS组及对照组,比较2组的肾素、血管紧张素、醛固酮水平及醛固酮肾素比值大小。结果:血管紧张素Ⅱ与血脂组分TC(r=0.329)、TG(r=0.936)及BMI(r=0.29)正相关,与HDL-C(r=-0.256)负相关,与LDL-C(r=0.116,P=0.111)无明显相关性,Logestic回归分析血管紧张素Ⅱ与高血压、高血糖、高血脂及代谢综合征均有明显相关性(P0.001),其中与MS回归系数最高(Exp(B)=1.082),MS组血清肾素、血管紧张素Ⅰ、血管紧张素Ⅱ、醛固酮水平均明显高于对照组(P=0.000),2组醛固酮肾素比值无差异。结论:RAAS水平与MS密切相关。     

动脉粥样硬化性肾动脉狭窄的治疗进展

肾血管性高血压主要是指继发于肾动脉狭窄而导致血压升高的一组疾病,是继发性高血压最常见的可治愈性疾病。肾动脉狭窄是一种进展性疾病,通常认为一侧或双侧肾动脉及其主要分支的狭窄达到或超过50%具有临床意义。