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抗心肌梗死
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     These results suggested that SM can enhance the cardioprotective effects of IP.
     结果表明,SM能加强IP的心肌保护作用,特别是加强IP的抗心肌梗死作用。
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     Objective A great deal of accumulated evidence implicate opening of mitochondrial ATP-sensitive potassium (MitoKATP) channel as an important step in the anti-infarct effect of ischemic preconditioning, it is the end-effector of preconditioning’s cardioprotection.
     目的:大量的研究证据表明, MitoKATP通道开放在预处理抗心肌梗死中起着非常关键的作用,它是预处理心肌保护的终末效应器。
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     The current and potential uses of the eight structural types of K ATP activators open a new field for developing the novel drugs against angina pectoris, cardiac ischemia and hypertension.
     依结构特征激活剂分8大类,对于研制新型抗心绞痛、抗心肌梗死和抗高血压药物开辟了一个新方向。
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     To quantify protected effect of norepinephrine (NE) induced delayed phase of ischemic preconditioning, the relationship between cardioprotection and superoxide dismutase(SOD) was studied.
     为定量去甲肾上腺素 (NE)诱导的延迟相预适应抗心肌梗死保护强度 ,研究了预适应机体抗氧化剂酶活性变化与预适应保护的关系。
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     sputum-resolving and mass-dispersing can improve the inadaptable myoeardial hypertrophy after Myocardiac infarction and reduce external stroma accumulation and fibrosis of eardiae museles. The long-term application can counteract the ventricular reconstruction.
     化痰散结可改善心肌梗死后心肌适应不良性肥厚和心肌外基质堆积和纤维化,长期使用可抗心肌梗死后心室重构。
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     Intervention with anti-H.
     H.
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     Anti-H.
     H .
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     Effects of Tongshu capsule on myocardial ischemia
     通舒胶囊的大鼠心肌梗死作用
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     Study on the Correlation of Anticardiolipin Antibody and Acute Myocardial Infarction
     心磷脂体与急性心肌梗死的相关性研究
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     Acute Atrial Myocardial Infarction
     急性心房心肌梗死
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ATP sensitive potassium channel (K ATP ) in cardiovascular system is an inward rectifier potassium ion channel which could be modulated by intracellular ATP concentration. K ATP is closely linked to membrane excitability and the bioenergetic states of the cell. Under physiological conditions it remains closed, while it plays an important regulatory role under hypoxic conditions. K ATP is highly K + selective with a single channel conductance of 80 and 135 pS in cardiomyocytes and vascular smooth...

ATP sensitive potassium channel (K ATP ) in cardiovascular system is an inward rectifier potassium ion channel which could be modulated by intracellular ATP concentration. K ATP is closely linked to membrane excitability and the bioenergetic states of the cell. Under physiological conditions it remains closed, while it plays an important regulatory role under hypoxic conditions. K ATP is highly K + selective with a single channel conductance of 80 and 135 pS in cardiomyocytes and vascular smooth muscles and opens in clusters of bursts separated by long close periods. Various factors known to regulate K ATP functions include channel gate, transducer unit, ATP binding inhibitory unit, presumed phosphorylation site and nucleoside diphosphate binding site. The dual effects of ATP on K ATP include the ligand actions and hydrolysis dependent actions. The first actions require the binding of ATP to the inhibitory unit to close the channels,while the second actions require phosphorylation of transducer unit caused by ATP in presence of Mg 2+ to restore the channel opening. Intracellular nucleoside diphosphate can antagonize the ATP induced inhibition of the channel opening and stimulate the channel to open. The pharmaco logical profiles of the three types of the channel activators depend on the channel functional states,especially nucleoside diphosphate binding site,presumed phosphorylation sites and inhibitory effects of ATP. The current and potential uses of the eight structural types of K ATP activators open a new field for developing the novel drugs against angina pectoris, cardiac ischemia and hypertension. Sulfonylurea drugs such as glibenclamide are selective K ATP antagonists. The molecular target of glibenclamide may be sulfonylurea receptors which belong to ATP-binding cassette protein family. More and more attentions have been paid to study the physiological actions of sulfonylurea receptors.

心血管ATP敏感性钾通道(KATP)是受细胞内ATP浓度调控的一种内向整流钾通道。在生理状态下,处于关闭状态;在缺氧的病理状态下,发挥重要的调节作用。心血管KATP对钾离子通透的选择性高,在心脏和血管平滑肌中其单通道电导分别为80和135pS,通道开放呈簇状并为长时间阻断状态所间隔。KATP功能性结构包括通道闸门、转换亚单位、ATP结合抑制亚单位、磷酸化位点和二磷酸核苷结合位点。ATP对KATP功能具有双向调节作用:其中配体作用是指与ATP结合抑制亚单位结合,使通道关闭;水解依赖性作用是指在Mg2+存在时,ATP使转换亚单位磷酸化,使通道开放。二磷酸核苷与其特异性位点结合,不仅降低通道对ATP的敏感性,而且可直接诱导通道开放。依对KATP作用特征激活剂分3大类,其药理作用依赖于通道的功能状态,尤其是磷酸化位点、二磷酸核苷结合位点和ATP的生物效应。依结构特征激活剂分8大类,对于研制新型抗心绞痛、抗心肌梗死和抗高血压药物开辟了一个新方向。以格列本脲为代表的硫脲类药物是KATP选择性拮抗剂,其作用环节可能是作用于硫脲受体后才发挥拮抗效应的,硫脲受体隶属ATP结合蛋白家族,其生理学作用已形成又一个研究热点

The role of injectio Salvia miltiorrhiza (SM) on enhancing the cardioprotective effects of ischemic preconditioning (IP) in anaesthetized rat was investigated. Results showed that IP reduced the severity of reperfusion-induced arrhythmia and limited the infarct size. SM limited the infarct size;SM+IP significantly reduced the infarct size as compared with IP alone;and significantly decreased both the infarct size and the severity of reperfusion-induced arrhythmia as compared with SM alone. These results suggested...

The role of injectio Salvia miltiorrhiza (SM) on enhancing the cardioprotective effects of ischemic preconditioning (IP) in anaesthetized rat was investigated. Results showed that IP reduced the severity of reperfusion-induced arrhythmia and limited the infarct size. SM limited the infarct size;SM+IP significantly reduced the infarct size as compared with IP alone;and significantly decreased both the infarct size and the severity of reperfusion-induced arrhythmia as compared with SM alone. These results suggested that SM can enhance the cardioprotective effects of IP.

以整体麻醉SD大鼠心脏冠状动脉左前降支结扎/松开作为缺血/再灌注动物模型,研究丹参注射液(SM)在加强缺血须处理(IP)的心肌保护中的作用。结果显示,IP能减轻复灌性心律失常的严重程度,缩小心肌梗死范围;SM能缩小心肌梗死范围;SM联合IP与单纯IP比较,心肌梗死范围进一步缩小;SM联合IP与单纯SM比较,心律失常严重程度减弱且心肌梗死面积进一步减小。结果表明,SM能加强IP的心肌保护作用,特别是加强IP的抗心肌梗死作用。

To quantify protected effect of norepinephrine (NE) induced delayed phase of ischemic preconditioning, the relationship between cardioprotection and superoxide dismutase(SOD) was studied. A total of 50 rats were randomly divided into three groups:NE group, I/R group and normal group, 3.1 μmol/kg NE was injected into abdomen 24 hours before surgery as a trigger, both NE and I/R group underwent main left coronary artery occlusion for 30 minutes then reperfusion for 120 minutes. Ischemic risk area, infarct area...

To quantify protected effect of norepinephrine (NE) induced delayed phase of ischemic preconditioning, the relationship between cardioprotection and superoxide dismutase(SOD) was studied. A total of 50 rats were randomly divided into three groups:NE group, I/R group and normal group, 3.1 μmol/kg NE was injected into abdomen 24 hours before surgery as a trigger, both NE and I/R group underwent main left coronary artery occlusion for 30 minutes then reperfusion for 120 minutes. Ischemic risk area, infarct area and nonischemic area were identified by TTC, Evan' s blue staining methods and calculated by Metamorph Imaging System software. Serum Cu 2+, Cytosol Cu 2+, Zn 2+-SOD content and activity, and activity of mitochondrial Mn-SOD activity were detected by radioimmunoassay and method xanthosine oxidase separately. Results showed that: 1) infarct size was reduced by 33.4% in preconditioned heart; 2) mitochondrial Mn-SOD activity was higher in preconditioned myocardium; 3) no significant difference about the activity and content of Cu 2+,Zn 2+-SOD either in serum or in myocardium was found. The above phenomena imply that preconditioned cardioprotection might be only related to mitochondrial Mn-SOD, mitochondrial Mn-SOD might be the final effector of NE induced preconditioning .

为定量去甲肾上腺素 (NE)诱导的延迟相预适应抗心肌梗死保护强度 ,研究了预适应机体抗氧化剂酶活性变化与预适应保护的关系。将 5 0只大鼠分为NE组、I/R组和正常组。 3.1μmol/kgNE腹腔内注射诱发预适应 ,2 4h后开胸结扎左冠状动脉主干 (LCA) ,造成LCA支配区缺血30min ,再灌注 12 0min复制预适应模型 ,用伊文斯蓝、TTC染色分别显示左室未缺血区、梗死区、危险区。数码相机与实体显微镜结合拍摄左室切面 ,MetamorphImagingSystem软件定量各组左室梗死区 /危险区面积 ,放免法和黄嘌呤氧化酶法分别测定血清Cu2 + 、胞浆Cu2 + ,Zn2 + -SOD含量、活性及线粒体Mn -SOD活性。结果显示 ,1)预适应保护可使心肌梗死面积减少 33.4 %;2 )预适应心肌线粒体Mn -SOD活性增高 ;3)血清及心肌细胞胞浆Cu2 + ,Zn2 + -SOD含量、活性预适应组与非预适应组差别不显著。实验研究启示 ,NE可诱导大鼠产生延迟相心肌预适应保护 ,其机制可能是通过使心肌线粒体Mn -SOD活性增高 ,减少自由基损伤 ,产生预适应保护。

 
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