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Objective To investigate the role of infiltrating CD4(superscript +)T cells in a rat model of ischemia-reperfusion injury.

目的 通过大鼠心肌缺血再灌注损伤的动物模型,分析CD4T细胞在心肌组织损伤中的作用。

Methods: Myocardial ischemia-reperfusion injury model was established through accluding the left anterior descending branch of coronary artery for 60 min and removing the ligation tater to reperfuse for 30 min.

结扎大鼠冠状动脉左前降支60min,再灌注90min复制大鼠心肌缺血再灌注损伤模型,观察心安灵对大鼠心肌缺血再灌注损伤的保护作用。

Objective To explore the protective effect of taurine on toxic cardiomyocytes induced by adriamycin and its mechanism.

目的 应用阿霉素建立心肌细胞中毒模型,观察牛磺酸对中毒心肌细胞的保护作用并探讨其机制。

The occurrence rate of major cardiovascular events (cardiovascular death, myocardial infarction, and re-building operation of blood flow for target vessel due to myocardial ischemia) and adverse reactions (hemorrhage , tetter, petechia , and reduction of white blood cells) were observed.

结果古稀组发生5例心血管事件(心肌梗死2例,靶血管再通3例);非古稀对照组发生6例心血管事件(心肌梗死3例,靶血管再通3例),两组间差异无统计学意义(P〉0.05);两组均无严重出血,其他副反应包括轻度上消化道出血、皮疹及瘀斑、轻度白细胞减少两组间差异无统计学意义(P〉0.05)。

Background Slowly activating delayed rectifier potassium currentI_(Ks is important in therepolarization of human cardiomyocyte action potential,especially in forming andmaintaining plateau of action potential. I_ channel is combined byαandβsubunits,which are coded by KCNQ1 and KCNE1 respectively. Mutations ofhKCNQ1/hKCNE1 genes,chronic myocardial hypertrophy and chronic heartfailure will lead to dysfunction of I_ and ingenital or acquired LQTS which areimportant factor in hazardous ventricular arrhythmia such as Torsade depoints.

实验背景缓慢激活延迟整流钾电流I_(Ks是参与人心肌细胞动作电位复极,特别是平台期形成与维持的重要外向离子流。I_通道由KCNQ1基因编码的α亚单位及KCNE1基因编码的β亚单位组成。hKCNQ1/hKCNE1基因突变或慢性心肌肥厚、慢性心力衰竭等病理过程均可导致I_功能异常,引起遗传性或获得性长QT综合征,LQTS易引起尖端扭转型室性心动过速等心律失常,从而危及病人生命。

Methods Men 50 health Chinese people accepted EBCT common transverse and short axis enhanced movie scan(27 men, 23 women, average age 47.7 years.).

方法50例健康人(男27例,女23例,平均年龄47.7岁),利用EBCT横断和心脏短轴电影扫描,分别测量主动脉、肺动脉、左心房和左心室径线,以及左心室心肌厚度、心肌增厚率等;利用心功能分析软件,计算左、右心室各功能指标。

Myocardialinfarct size and the area at risk for myocardial infarctionwere measured by Evans Blue and triphenyl tetrazolium chloridestaining, respectively.

心肌梗死面积和可能发生心肌梗死的危险区分别可以用偶氮蓝与氯化三苯四唑染色测量。

The area at risk and infarct area were determined using Trypan blue and triphenyl tetrazolium choride staining respectively.

再灌末取心肌组织,以四氮唑染色法测定心肌梗死面积(IS/AAR×100%)。

TSN can prevent the hypertrophy of cardiomyocytes induced by Ang Ⅱ, which may relate to the depress of cardiomyocyte apoptosis by TSN.

TSN可以抑制Ang Ⅱ诱导的心肌细胞肥大,这可能与其同时抑制了心肌细胞的调亡有关。

Aim: To determine whether activation of κ-opioid receptor with U50,4 88 H, a selective κ-opioid receptor agonist, produces any changes in electrical u ncoupling during prolonged ischemia and whether these changes in electrical unco upling is associated with the cardioprotection induced by κ-opioid receptor ac tivation, and to explore the possible mechanism.

测量指标:以分光光度计在490nm波长下测定氯化三苯基四氯唑与活细胞反应的产物formazan含量的方法测定心肌细胞活性、测定冠脉流出液中乳酸脱氢酶的含量以及心室内压;②全心停灌70min,应用四电极法观察不同浓度U50,488H、nor-BNI和5-HD对缺血期间心肌整体阻抗和电脱耦联参数(电脱耦联时间、平台时间、电脱耦联最大速率和阻抗倍数)的影响。

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