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腹主动脉缩窄

腹主动脉缩窄的相关文献在1989年到2022年内共计88篇,主要集中在内科学、中国医学、基础医学 等领域,其中期刊论文82篇、会议论文5篇、专利文献77731篇;相关期刊61种,包括现代生物医学进展、中国病理生理杂志、岭南心血管病杂志等; 相关会议5种,包括2014北京大学心血管转化医学论坛、第八次全国中西医结合基础理论研究学术研讨会、江苏省药理学会第六届学术研讨会等;腹主动脉缩窄的相关文献由327位作者贡献,包括刘杰、刘永明、初楠等。

腹主动脉缩窄—发文量

期刊论文>

论文:82 占比:0.11%

会议论文>

论文:5 占比:0.01%

专利文献>

论文:77731 占比:99.89%

总计:77818篇

腹主动脉缩窄—发文趋势图

腹主动脉缩窄

-研究学者

  • 刘杰
  • 刘永明
  • 初楠
  • 史旭波
  • 李田昌
  • 杨进刚
  • 王文
  • 胡大一
  • 马力
  • 刘丽
  • 期刊论文
  • 会议论文
  • 专利文献

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    • 周瑞; 黄河; 刘应才
    • 摘要: 目的 探讨伊伐布雷定对心肌肥厚大鼠超极化激活环核苷酸门控非选择性阳离子通道(HCN)和交感神经的影响.方法 18只雄性SD大鼠分为假手术组(Sham组)、模型组和伊伐布雷定组(IVA组),每组6只.模型组和IVA组行腹主动脉缩窄术,术后12周IVA组予以10 mg·kg-1·d-1的伊伐布雷定灌胃,Sham组和模型组予以等体积生理盐水灌胃.17周后处死大鼠,测定全心质量指数、左心室质量指数,苏木素-伊红(HE)染色评估心肌肥厚水平,免疫组织化学检测心肌HCN和酪氨酸羟化酶(TH),Western blot和PCR检测HCN蛋白和mRNA水平,ELISA法检测心肌组织去甲肾上腺素(NA)和肾上腺素(EPI)水平.结果 与Sham组比较,模型组、IVA组全心质量指数、左心室质量指数增加,差异有统计学意义(P<0.05).Sham组心肌细胞规则紧密;模型组心肌细胞变长,细胞核体积增加,排列稀疏、不规则;IVA组心肌细胞排列基本整齐.Sham组心肌细胞少量表达HCN2、HCN4,模型组HCN2和HCN4表达水平较Sham组明显增加,IVA组较模型组减少(P<0.05).与Sham组比较,模型组TH分布及NA、EPI表达明显增加,而IVA组TH分布及NA、EPI较模型组表达减少(P<0.05).结论 伊伐布雷定能抑制心肌肥厚大鼠HCN及交感神经的表达.
    • 臧茂林; 余梦迪; 陈重华; 黄梦琪; 罗鹏; 樊红琨; 杨春
    • 摘要: 目的:探讨腹主动脉缩窄小鼠在向心衰发展的过程中心脏结构和功能的动态变化.方法:健康雄性昆明小鼠,随机分为模型组、假手术组和对照组.模型组采用腹主动脉缩窄的方法制备慢性心力衰竭小鼠模型,假手术组只分离出腹主动脉但不结扎,对照组不做任何处理.模型组组内分为2周组、4周组、6周组和8周组,每组10只.观察各组小鼠行为学表现、心电图、超声心动图和心肌组织病理学的变化.结果:模型组与对照组相比:模型组小鼠术后2周开始出现行为学改变并且仅有2周组小鼠出现IVSS降低(P<0.05);术后4周开始出现病理性J波、EF降低(P<0.05)、IVSD增加(P<0.05)和心肌损伤;术后6周开始出现LVPWD和LVPWS增加(P<0.05);术后8周开始出现LV mass corrected增加(P<0.05).各组小鼠心率、R幅值、T幅值、ST段、PR间期、QT间期、QTc等数据差异均无显著性.结论:腹主动脉缩窄导致小鼠出现心衰的过程中出现了EF降低、室间隔肥厚、病理性J波、左室后壁肥厚以及左室质量增加等变化.
    • 谭巍; 任澎
    • 摘要: 目的 通过研究不同程度缩窄腹主动脉对Wistar大鼠心脏功能的影响,建立大鼠心衰模型.方法 将Wistar大鼠随机分成3组,A组为假手术组,B组缩窄腹主动脉直径至0.45 mm,C组缩窄腹主动脉直径至0.7 mm,术后观察大鼠生存情况、精神状态等一般情况,在4周和8周分别应用超声心动图检测舒张末期室间隔厚度(IVSd)、舒张末期左室后壁厚度(LVPWd)、左室舒张末期内径(LVEDd)、左室收缩末期内径(LVEDs)和射血分数(LVEF),并取标本测量左心室质量指数LVWI、心/体比、肺/体比,评价心功能的变化.结果 术后A组存活率为100%,B组存活率为55%,C组存活率为70%;4周时B组IVSD、LVPWd、LVEDd、LVEDs、LVEF与A组和C组均有显著差异(P<0.05),C组与A组相比IVSD、LVPWd、LVEDs有所增加,而LVEDd、EF差异无统计意义(P>0.05).8周时B、C两组IVSD、LVPWd、LVEDd、LVEDs、LVEF与A组相比差异显著(P<0.05);8周时LVWI、心/体比、肺/体比B组和C组分别与A组相比均有极显著差异(P<0.01),C组与B组相比LVWI、心/体比有显著差异(P<0.05),肺/体比差异极显著(P<0.01).结论 腹主动脉缩窄至直径0.45 mm比缩窄至0.7 mm心衰成模所需时间短,成模效率高,是建立大鼠心衰模型的理想方法.
    • 刘成芳; 刘继斌; 王瑾; 和荣丽; 孔丽; 吴博威
    • 摘要: 目的:研究心肌内向整流钾电流(IK1)激动剂扎考比利对腹主动脉缩窄后大鼠心功能及心肌纤维化的改善作用.方法:腹主动脉缩窄造成大鼠压力超负荷心室重构模型,将建模成功的80只大鼠通过随机数字表分为模型组、扎考比利组、氯喹组、扎考比利+氯喹组(每组20只),后三组依次预防性给予扎考比利、IK1阻断剂氯喹、扎考比利+氯喹.另设假手术组(n=10),开腹后只挂线,不结扎.连续给药8周后,采用血流动力学指标评价各组大鼠心功能,放射免疫学方法测定血浆B型利钠肽(BNP)和肿瘤坏死因子-α(TNF-α)水平,马松染色观察心肌间质胶原沉积,免疫组织化学法测定心肌组织Ⅰ型、Ⅲ型胶原的表达并计算胶原Ⅰ型/Ⅲ型胶原比值,逆转录聚合酶链反应法检测心肌组织转化生长因子-β1(TGF-β1)、Smad3和Smad7信使RNA(mRNA)表达.结果:与模型组相比,扎考比利组大鼠左心室收缩压(LVSP)、左心室压力上升最大速率(+dP/dtmax)、左心室压力下降最大速率(-dP/dtmax)均显著升高,左心室舒张末期压力(LVEDP)显著降低,血浆BNP和TNF-α水平显著降低,心肌间质胶原面积明显减小,Ⅰ型、Ⅲ型胶原表达下降,且Ⅰ型/Ⅲ型胶原比值显著降低,心肌组织TGF-β1、Smad3 mRNA表达明显降低,Smad7 mRNA表达明显升高,差异均有统计学意义(P均<0.05).氯喹组和扎考比利+氯喹组上述各项指标与扎考比利组相比,差异均有统计学意义(P均<0.05),变化趋势与扎考比利组和模型组比较的上述结果相反.结论:扎考比利能够明显改善腹主动脉缩窄后大鼠的心功能与心肌纤维化程度,其机制可能与TGF-β1/Smads信号通路有关.
    • 符镇洋; 孙一帆; 姜成; 黄蕾; 林吉进
    • 摘要: 目的 研究大鼠心肌肥厚时FHL2表达水平的变化,探讨FHL2对心肌肥厚调控的作用.方法将雄性SD大鼠20只,随机分成腹主动脉缩窄组( AAC组)和假手术组( Sham组),每组10只,AAC组通过U型银夹缩窄腹主动脉的方法建立左室心肌肥厚模型,Sham组进行相同的手术步骤但未缩窄腹主动脉;术后6周,经胸心脏彩超测定心脏形态和心功能后以颈椎脱臼法处死,分离大鼠心脏记录形态学参数并通过 HE染色和Masson染色观察心脏形态和纤维化程度;提取所有心肌组织总蛋白和总RNA,采用Western blot技术、实时定量PCR技术分析FHL2在两组大鼠心肌组织中的蛋白和 mRNA表达水平.结果 术后6 周,心脏超声结果显示ACC组心肌较Sham组明显肥厚(P<0.05);与Sham组相比,AAC组大鼠心肌组织明显增厚,差异有统计学意义( P <0.05);ACC 组 FHL2 蛋白和 mRNA 水平均明显较 Sham 组升高,差异有统计学意义(P<0.01).结论 心肌肥厚时FHL2表达水平明显上调;FHL2 可能在心肌肥厚的发生发展过程中发挥重要调节作用.%Objective To study the expression of FHL2 rats with cardiac hypertrophy .Methods Twenty male Sprague-Dawley (SD) rats were randomly divided into the abdominal aortic constriction group (Group AAC, n=10) and Sham group (Group Sham, n=10).The left ventricular hypertrophy model was established by implanting silver U clip on abdominal aorta in Group AAC , the same procedure except for silver U clip implanting was done in Group Sham . Transthoracic echocardiography was performed to detect the myocardial morphology and function 6 weeks after operation . The rats were sacrificed by cervical vertebra dislocation , and the hearts were harvested to measure the weight and analysis the relevant ratio.In addition, the myocardial tissues were detected in morphology with HE staining and Masson staining . The Western blot and real -time quantitative PCR analyze were used to detect the protein expression level and mRNA level of FHL2 in myocardial tissues .Results Compared with the Group Sham , there was a dynamic change of hypertrophy in Group ACC with a significant difference ( P<0.05).The histological examination also showed significant increasing of cardiac hypertrophy in ACC group (P<0.05).Both the protein and mRNA levels in Group ACC were significantly higher than those in Group Sham.Conclusion The expression of FHL2 is significantly up-regulated in hypertrophic myocardi-um.FHL2 may play an important role in the development of cardiac hypertrophy .
    • 陈洪; 黄波; 李世月; 徐云燕; 邓江; 吴芹; 石京山
    • 摘要: 目的 观察吴茱萸次碱(rutaecarpine,Rut)对压力超负荷所致大鼠左心室结构及功能的影响.方法 通过腹主动脉缩窄术(abdominal aortic constriction,AAC)制作心肌肥厚模型,造模4周后,随机分为AAC组、吴茱萸次碱低、高剂量组(10、20 mg/kg/d,po)和假手术(Sham)组.连续给药4周后测量大鼠尾动脉血压,并利用高分辨率小动物超声系统检测大鼠心脏结构和功能改变;分离组织计算左心室肥厚指数(LVHI);H&E染色观察左室心肌组织形态学变化;qRT-PCR法检测心肌心房钠尿肽(atrial natriuretic peptide,ANF) mRNA表达.结果 与Sham组比较,AAC大鼠血压明显升高(P<0.05),LVHI显著增加;超声结果显示左室前壁(LVAW)和后壁(LVPW)厚度均大于Sham组(P<0.05);而收缩及舒张期左室内径(LVID)低于Sham组;心功能指标左心室收缩末期心室容积(LV Vol.s)及舒张末期心室容积(LV Vol.d)和每搏输出量(SV)小于Sham组(P <0.05,P<0.01),表明左室肥厚且收缩与舒张功能出现异常.H&E染色显示AAC组心肌细胞排列紊乱且细胞间隙增宽,伴有肌丝部分断裂;心肌组织ANF mRNA表达明显增加;给予吴茱萸次碱低、高剂量治疗后,血压显著降低(P<0.05),LVHI明显减小;收缩期及舒张期LVAW及LVPW显著下降(P <0.05,P<0.01),同时收缩及舒张期LVID和LV Vol.及SV的值增大(P <0.05,P<0.01),表明吴茱萸次碱可有效改善左心室结构和心肌收缩舒张功能障碍;H&E染色观察发现心肌细胞排列趋于整齐且细胞间隙缩窄,未见明显肌丝断裂;同时下调心肌ANF mRNA水平的表达(P<0.05).结论 吴茱萸次碱可显著改善腹主动脉缩窄术所致大鼠左室结构及心功能损害.%Objective To evaluate the efficacy of rutaecarpine (Rut)on left cardiac structure and function in rats with myocardial hypertrophy induced by pressure overload.Methods A rat model of myocardial hypertrophy was induced by abdominal aortic constriction(ACC).Rats were randomly divided into four groups:Sham group,AAC group,low dose (10 mg/kg,p.o.) of Rut group (Rut-L) and high dose (20 mg/kg,p.o.) of Rut group (Rut -H).The blood pressure of tail artery was measured before and after Rut treatment.The cardiac structure and function were detected by high resolution ultrasound imaging system (HRUIS).The myocardial pathology was examined by H&E staining.The left ventricular hypertrophy index(LVHI) was calculated.The level of atrial natriuretic peptide(ANF) mRNA was detected by qRT-PCR.Results The blood pressure was significantly increased in ACC group.HRUIS revealed that ACC increased systolic and diastolic left ventricular anterior wall(LVAW) thickness,left ventricular posterior wall (LVPW)thickness,left ventricular internal diameter(LVID) and average cardiac stroke volume(SV).Also,ACC increased LVHI and disorganized cardiomyocytes with widening of cell gap and partial rupture of muscle fibers,and increased ANF mRNA.After Rut treatments,AAC-elevated blood pressure was decreased,the LVID was narrowed,and the LVAW,LVPW and LVHI were decreased,while the LV Vol.and SV were increased.Cardiomyocyte hypertrophy was improved and the elevated ANF returned towards the normal level.Conclusion Rut could improve the AAC-induced left cardiac structure changes and function damage in rats.
    • 鲁成; 刘永明; 陈启松
    • 摘要: 目的 通过心脏彩色多普勒超声评价腹主动脉缩窄大鼠的心脏功能及潜阳合剂的干预作用.方法 选取清洁级雄性Wistar大鼠40只,按随机数字表分为假手术组、模型组、中药组、培哚普利组,并行相应腹主动脉缩窄术或假手术,每组各10只.造模后8周开始药物干预,共干预12周.观察药物干预对外周血压、左心室肥厚以及左室功能的影响.结果 造模20周后,模型组收缩压(SBP)明显升高(P<0.05),中药组和培哚普利组SBP低于模型组(P<0.05).模型组大鼠室间隔厚度(IVSd)显著增高(P<0.05),中药组和培哚普利IVSd均小于模型组(P<0.05).模型组二尖瓣舒张早期流速峰值(E峰)显著减小(P<0.05);中药组E峰大于模型组(P<0.05).模型组E/A比值显著降低(P<0.05),中药组E/A比值大于模型组(P<0.05).结论 心脏彩色多普勒超声是评价腹主动脉缩窄大鼠心脏功能的有效方法.潜阳合剂可有效降低腹主动脉缩窄大鼠的外周血压,抑制左心室肥厚,并能改善左室舒张功能.
    • Qiu Jiantao; Shi Guangjun; Xiao Huaiteng; Cheng Yayu; Tan Xueying
    • 摘要: Objective To explore the effects and mechanisms of tanshinone Ⅱ A (Tan Ⅱ A) on cardiac hypertrophy in rats.Methods 40 SD rats of 2-3 months old were randomly divided into four groups with 10 in each group,transverse aortic constriction (TAC) was used to simulate pressure-overload models.The four groups were handled as follows,the sham group rats just underwent laparotomy;the surgery group were exposed to TAC as TAC group;the Tan Ⅱ A group rats were administered Tan Ⅱ A (20 mg· kg-1· d-1) by intraperitoneal injection for 8 weeks after TAC;the negative control group rats were given normal saline (20 mg· kg-1 · d-1) by intraperitoneal injection for 8 weeks after TAC.After 8 weeks of TAC,we randomly chose 6 rats from each group and anaesthetized them.Echocardiogram was performed to evaluate cardiac structure and function.After measuring body weight,the chosen rats were dissected and their heart weight were measured to calculate heart-weight index (HWI).The acquired heart tissue was used to produce frozen sections performed with hematoxylin and eosin (HE) staining and Masson staining to evaluate cell surface area (CSA) and collagen volume fraction (CVF),respectively.Western blot analysis was performed to evaluate calcium/calmodulin-dependent protein kinase Ⅱ (CAMK Ⅱ) and calcineurin (CAN) protein expression in rat heart tissue.Results Compared to TAC group,Tan Ⅱ A group rats had lower left ventricular posterior wall thickness (LVPWd) and interventricular septum thickness (IVSd) [LVPWd:(0.2± 0.01) cm vs (0.22±0.01) cm,P<0.05;IVSd:(0.18±0.02) cm vs (0.22±0.02) cm,P<0.05].HWI was also lower in Tan Ⅱ A group compared with TAC group [(43.43:±5.10) mg/g vs (49.38±3.80) mg/g,P<0.05].The staining results showed Tan Ⅱ A significantly inhibited myocardial hypertrophy and fibrosis caused by TAC[CSA:(555.48±879.81) μm2 vs (514.74± 1281.16) μm2,P<0.05;CVF:(8.63%±2.26% vs 12.39%± 1.90%,P<0.05)].Western blot analysis demonstrated that Tan Ⅱ A could reduce the elevation of CAMK Ⅱ and CaN protein expression resulted from TAC[CAMK Ⅱ:(1.2±0.1) vs (1.83±0.25),P<0.05;CaN:(1.27±0.12) vs (1.93±0.49),P<0.05].Conclusion Tanshinone Ⅱ A could inhibit pressure-overload induced myocardial hypertrophy in rats.%目的 研究丹参酮ⅡA对大鼠心肌肥厚的影响及相关机制.方法 将40只2~3月龄的SD大鼠随机分为4组,每组10只.应用腹主动脉缩窄术(TAC)制造压力负荷模型.4组大鼠分别做如下处理:对假手术组只开腹不作特殊处理;对手术处理组行TAC(TAC组);对丹参酮ⅡA干预组行TAC后,给予腹腔注射丹参酮ⅡA8周(20 mg· kg-1·d-1);对阴性对照组行TAC后,给予腹腔注射生理盐水8周(20 mg℉kg-1·d-1).8周后从各组随机选取6只小鼠,对小鼠麻醉后行超声心动图检查评估心脏结构和功能;测量小鼠体重后进行心脏取材,测量心脏重量,计算大鼠心脏重量指数(HWI);制作心肌组织切片,进行苏木精-伊红染色(HE)和Masson染色,检测心肌细胞横切面积(CSA)以及胶原体积分数(CVF);用免疫印迹法检测心肌组织钙调蛋白激酶Ⅱ(CAMKⅡ)和钙调神经磷酸酶(CAN)的蛋白表达水平.结果 对比TAC组,丹参酮ⅡA组大鼠左心室后壁舒张末厚度(LVPWd)和室间隔舒张末厚度(IVSd)均显著下降[LVPWd:(0.2±0.01)cm比(0.22±0.01) cm,P<0.05;IVSd:(0.18±0.02) cm比(0.22±0.02) cm,P<0.05],HWI下降[(43.43±5.1) mg/g比(49.38±3.8) mg/g,P<0.05];组织染色结果显示,丹参酮ⅡA干预组显著降低了TAC引起的CSA和CVF升高[CSA:(555.48±879.81) μm2比(514.74±1 281.16) μm2,P<0,05;CVF:(8.63%±2.26%比12.39%±1.9%,P<0.05)];免疫印迹法结果提示,丹参酮ⅡA组大鼠较TAC组心肌组织内CAMKⅡ和CaN的蛋白表达量显著下降[CAMKⅡ:(1.2±0.1)比(1.83±0.25),P<0.05;CAN:(1.27±0.12)比(1.93±0.49),P<0.05].结论 丹参酮ⅡA能抑制压力负荷引起的心肌肥厚.
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