- 更多网络例句与心肌相关的网络例句 [注：此内容来源于网络，仅供参考]
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Combined with animal model of peradaptation to myocardium ischemia , the research observed the level of enzymatic dynamics of myocardium, SOD,MDA,ET and correlation peptide of calcitonin gene in peripheral blood and cardiac function, apoptic cell and expression of apoptosis regulatory gene, ultrastructure of myocardium with BIOPAC16, in situ end labeling and hybridism, optic microscope and electron microscope. The study of animal model of peradaptation to myocardium ischemia illustrated that the peradaptation and pretreatment with Wenxin capsule could be positively protective for the injury of ischemia reperfusion. The protection is mainly reflected by reduction of infarction area, correction of heart rhythm abnormality of ischemia reperfusion, melioration of the contraction and relaxation function of myocardium, recovery of the subcellular structure and themelioration of the abnormality of biochemical and bioactive substance in the myocardium.
并结合心肌缺血预适应动物模型，采用BIOPAC16导生理记录和分析处理系统处理心肌功能指标，采用原位末端标记及原位杂交技术标记凋亡细胞及凋亡相关调控基因的表达，采用光电镜技术观察心肌超微结构的变化，同时观察外周血心肌酶、超氧化物歧化酶、丙二醛、内皮素、降钙素基因相关肽等水平，结果表明心肌缺血预适应及温心胶囊预处理对心肌缺血再灌注损伤具有肯定的保护作用，其保护心脏作用主要表现在缩小心肌梗死范围、抗缺血再灌注心律失常、改善心肌收缩和舒张功能、减轻心肌超微结构损伤，调节心肌生化物质及生物活性物质的生成和释放。
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Based on the latest achievements of the mechanism of peradaptation to myocardium ischemia and pharmacodic preadaptation up to date, observations were made on 80 patients of acute myocardial infarction to assess the enzymatic dynamics of myocardium, symptoms after myocardial infarction occurred like cardiac rhythm abnormality, anginapectoris, heart failure, cardiogenic shock, reinfarct and the mortality in the hospital. The results indicated that peradaptation to myocardium ischemia is of significance in protecting myocardium, reducing the areas of infarction, abating the cardiac insufficiency after infarction and reducing the abnormality of heart rhythm and significantly ameliorating the prognosis.
本研究结合现代医学对心肌缺血预适应机制及药理性预适应作用的最新研究成果和动向，通过临床观察80例急性心肌梗死患者的心肌酶学变化，心律失常、梗死后心绞痛、心力衰竭、心源性休克、再次梗死等心肌梗死后并发症和住院病死率，证实缺血预适应具有保护心肌，缩小梗死范围，减轻梗死后心功能不全及减少心律失常的作用，可明显改善心肌梗死病人的预后。
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HISI treatment prolong the survival time of mice in toxic condition induced by sodium nitrite and duration of electrocardiograph in trachea closed mice .HISI could obviously improve the ischemic electrocardiogram T-wave induced by Pituitrin.ST segment drifts on electrocardiogram in acute myocardial ischemia rats induced by Isoprotereno were obviously opposed by administration of HISI. The myocardial infarction areas, releasement of lactic dehydrogenase 、 creatine phosphokinase significantly increased in myocardial ischemia dogs, HISI treatment prevented these effects .
实验结果表明：苦碟子氯化钠注射液能显著延长小鼠常压缺氧环境及亚硝酸中毒情况下的存活时间，延长小鼠气管夹闭后心电消失时间；可显著改善垂体后叶素诱发的大鼠急性心肌缺血心电图T波异常；明显对抗异丙肾上腺素诱导的急性心肌缺血大鼠心电图ST段的偏移；显著改善冠脉结扎所致急性心肌缺血犬的心外膜心电图缩小其梗死心肌面积，降低心肌耗氧量，减少心肌坏死导致的心肌酶如乳酸脱氢酶、肌酸磷酸激酶的漏出。
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Adenovirus 5第二军医大学博士学位论文英文摘要胸心外科专业(WAd5) and PDC-MLC-VEGF were transferred to the adenoviral packaging cell HEK 293cell by lipofectamine 2000 mediated gene transfer method to pack the virus; The desired Advectors were purified by density gradient ultracentrifuge and titrated in 293 cells afteridentified.
Ad.mlc-hVEGF165 体外转染心肌细胞的实验研究分离培养乳鼠心肌细胞，在同一 MOI 值下，Ad.mlc-hVEGF165 和 Ad.hVEGF165分别转染心肌细胞，以 RT-PCR 法和 Western 印迹分析法分别检测转染后心肌细胞内VEGF mRNA 的转录及 VEGF 蛋白的表达，以 ELISA 法检测转染后心肌细胞分泌的VEGF 蛋白质，MTT 等方法观察其对促内皮细胞增殖作用。
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Cardiac hypertrophy is one of adaptive responses of the heart to a variety of pathological stimuli, including hypertension, myocardial infarction, congenital heart disease, heart valvula disease, and perturbations in sarcomeric function due to altered expression or mutations of contractile proteins. Increase in wall tension and hormonal stimuli are thought to directly activate various membrane-bound receptors and signal transduction cascade within cardiomyocytes resulting in the activation of immediate early genes and responsive genes such as c-jun, c-fos, c-myc, egr-1, ANF, BNP. Then the expression of construction proteins such as MLC-1, skeletal α-actin was unregulated.
中文题名hhlim基因的表达调节及其与心肌细胞肥大发生之间的关系副题名外文题名 hhlim gene expression regulation and its role in development of cardiomyocyte hypertrophy 论文作者郑斌导师温进坤韩梅学科专业生物化学与分子生物学研究领域\研究方向学位级别博士学位授予单位河北医科大学学位授予日期2003 论文页码总数106页关键词心肌细胞肥大基因表达心肌肥厚 hhlim基因馆藏号BSLW /2003 /R542.2 /33 心肌细胞肥大是高血压、心脏瓣膜病、急性心肌梗塞及先天性心脏病等临床常见疾病的一种并发症，是心肌细胞对多种病理刺激的一种适应性反应。
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Results: It was found that the myocardial chymase-like activity increased markedly in hypertrophied rat (2,6,12 weeks);the angiotensinⅡand aldosterone contents increased significantly in hypertrophied rat (12 weeks);and the myocardium angiotensin Ⅱ,aldosterone levels correlated positively to the myocardium chymase- like activity .
结果：术后2、6、12周心肌肥厚组大鼠心肌组织糜酶样活性较同期正常对照组显著增高（P＜0.01）；术后12 周心肌肥厚组大鼠心肌血管紧张素Ⅱ、醛固酮含量较同期正常对照组明显增加（P＜0.01）；心肌组织血管紧张素Ⅱ、醛固酮水平与糜酶样活性呈正相关（P＜0.05）。
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The cardiomyocyte viability were detected by MTT assay for calculating the survival rate and the inhibitory rate of the virus. Myocardial F-actin and VEGF were analyzed by immunofluorescent staining with confocal microscopy. Mean fluorescent intensity of F-actin and VEGF were determined by flow cytometry.Results There is no toxicity on cardiomyocytes when PD is at concentration of 0.02 mmol/L and 0.2 mmol/L while there is toxicity at concentration of 2 mmol/L. CVB3 could reduce the viability of cardiomyocytes, depolymerize F-actin cytoskeleton and reorganize VEGF protein.
体外培养心肌细胞，用100 TCID50柯萨奇B3病毒（CVB3）感染心肌细胞，建立病毒性心肌炎实验模型，然后分别用0.02mmol/L、0.2mmol/L、2mmol/L三种不同浓度的PD处理感染CVB3病毒的心肌细胞，观察心肌细胞的形态和搏动，用细胞免疫荧光技术标记纤维状肌动蛋白和VEGF蛋白，四唑蓝比色法测定心肌细胞活性和病毒抑制率，流式细胞仪检测各组心肌细胞VEGF蛋白和F-actin平均荧光强度。
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CaN Aβ gene silencing can reduce myocardial hypertrophy in cultured cells, si1280 (21bp) of CaN Aβ gene is the most effective target site for siRNA. The method of intrapericardial injection of plasmid, microbubbles and erzymes can improve transfection efficiency of non-viral plasmid with satisfying targeted transfection. But the scope of transfected myocytes is still limited. CaN Aβ shRNA expressing plasmid transfection in vivo by pericardial injection results in decreased CaN Aβ protein expression of small part of myocytes, and CaN Aβ mRNA only shows decreased trend. The dosage of non-viral vector and the parameters of ultrasound energy should be optimized in further study.
结论RNAi技术抑制CaN Aβ基因表达可有效减轻Ald诱导的心肌细胞肥大程度；CaN Aβ基因中si1280(21bp)片段为实现RNAi的更有效片段；微泡+酶类心包腔内注射超声导入的方法可有效改善非病毒载体在体心肌的转染效率，同时具有一定的靶向性，但总的转染范围仍然有限；采用这一方法进一步进行&一肾一夹&心肌肥大模型大鼠在体心肌细胞的CaNAβ的RNAi干预，发现心肌肥大大鼠心外膜下局部心肌细胞CaN Aβ蛋白水平降低，CaN AβmRNA水平虽有下降趋势，但无统计学差异，提示质粒的用量及超声导入的参数有待进一步研究使其优化。
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Reduce the hoist of leucocytes of sinus coronaries blood of myocardial ischemia and reperfusion injury dogs;2. decrease the leakage of plasma CK, CK-MB and LDH;3. regulate the vaso-active substances such as ET, TXB〓 and PGI〓;4. decreased the inflammatory cell factors such as IL-1, IL-6 and TNF
综上，奥沙恩注射液可降低心肌缺血再灌注损伤模型犬冠状窦血白细胞总数，减少I／R后CK、CK-MB和LDH的释放，调节血管活性物质ET、〓和〓的产生，降低血清炎性细胞因子TNF-α、IL-1和IL-6的含量，抑制PMN的激活及对心肌的浸润，减轻心肌组织的病理改变，以及减轻心肌缺血及坏死程度、降低心肌耗氧量，从而显示出较强的对犬急性心肌缺血再灌注损伤的保护作用。
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Measurirg indxes included:(1) Electrocardiograh;(2) Hemodynamics: cardiac output, pump output, aortic pressire, pulmo nary artery pressure, left atrium pressure, right atrium pressure, left ventricular end systolic pressure, left ventricular end diastolic pressure, LV-dp/dt, right ventricul ar end systolic pressure, RV-dp/dt, systolic pressure time index, diastolic pressure time index, endocardial viability ratio;(3) Myocardial metabolism: coronory sinus blood flow, myocardial oxygen consumption, myocardial lactate extractiorn;(4) Ischemic myocardial area;(5) Ultrastructure of myocardium.
测量指标包括：①心电图；②血流动力学：心输出量、泵输出量、主动脉压、肺动脉压、左房压、右房压、左室收缩末压、左室舒张末压、左室压的一阶导数、右室收缩末压、右室压的一阶导数、收缩压力时间指标、舒张压力时间指标、心内膜下心肌供血比率；③心肌代谢；冠状窦血流量、心肌氧耗量、心肌乳酸摄取量；④心肌缺血面积检查及缺血心肌的超微结构观察。
- 更多网络解释与心肌相关的网络解释 [注：此内容来源于网络，仅供参考]
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cardiac muscle：心肌
肌纤维的细胞膜称肌膜(sarcolemma),细胞质称肌浆(sar二、心肌 心肌(cardiac muscle)分布于心脏和邻近心脏的大血管近段. 心肌收缩具有自动节律性,缓慢而持久,不易疲劳. (一)心肌纤维的光镜结构 心肌纤维呈短柱状,多数有分支,相互连接成网状.
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myocardial hibernation：心肌冬眠
更长时间的心肌血供完全中断(大于30min),则造成心肌细胞不可逆性损伤、坏死, 即心肌梗死(myocardial infarction);慢性心肌缺血供血不足,当血供恢复正常后,心肌功能可部分或全部恢复正常, 即心肌冬眠(myocardial hibernation).
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cardiac hypertrophy：心肌肥厚
心肌肥厚(cardiac hypertrophy)是指心肌细胞增大而无细胞分裂,是心肌细胞对高血压、瓣膜病、急性心肌梗塞及先天性心脏病等常见临床疾病的一种基本应答. 由于人出生后不久心肌细胞就失去分裂的能力,所以成年心肌细胞只能以这种机制来适应负荷的增加.
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myocardial infarction：心肌梗死
心肌梗死(myocardial infarction)是指冠状动脉突然发生完全闭塞或近乎堵塞,血流急剧减少或中断,使相应的心肌严重而持久地急性缺血致心肌缺血性坏死. 临床上产生剧烈而持久的胸痛和对组织坏死的一些全身性反应,血清心肌酶活力增高和心肌急性损伤与坏死的心电图进行性演变变化,
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myocardium：心肌膜
2.心肌膜 心肌膜(myocardium)主要由心肌构成,心房的心肌较薄,心室的心肌很厚,左心室的最厚. 心肌纤维呈螺旋状排列,大致可分为内纵、中环和外斜三层. 心肌纤维多集合成束,肌束间有较多的结缔组织和丰富的毛细血管.
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myocardium：心肌细胞
心脏主要由心肌细胞(Myocardium)组成. 心肌细胞分布不单在心壁上,临心大血管上也有心肌的分布. 心肌也是横纹肌. 相比起骨骼肌细胞,心肌细胞有其自身的特点: 自律心肌细胞具有自律性. 即使离体的心脏仍表现出自律的舒张收缩活动.
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stunned myocardium：顿抑心肌
三者 均可引起可逆性左室功能障碍. 随着挽救缺血心肌的介入治疗及冠脉搭桥术临床应用的日益 增多,心肌存活性的鉴定在缺血性心脏病治疗决策中愈显重要. 现就心肌存活性及其评价技 术的进展作一综述. 1.1 顿抑心肌(Stunned Myocardium)或心肌顿抑
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Hibernating myocardium：冬眠心肌
然而,近年来的研究已证明由于心肌缺血的速度、程度不同,以及缺血心肌有无再灌注或侧支循环供血,心肌梗死(MI)后的RWMA区域除了坏死心肌外,还可能有下列存活心肌(viable myocardium)存在:1.顿抑心肌(stunned myocardium);2.冬眠心肌(hibernating myocardium);3.伤残心肌(m
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Hibernating myocardium：心肌冬眠
慢性心肌缺血,心肌收缩功能受到抑制,当血供恢复以后而心功能、生化及超微结构异常仍持续存在称之为心肌冬眠(hibernating myocardium),它也是心肌对慢性缺血一种调节机制和心肌对缺血时降低做功、减少氧耗、最大限度地维持心肌存活,
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stunning：心肌顿抑
冠心病心肌缺血可能导致三种结果,即:心肌顿抑(stunning)、心肌冬眠(hibernating)和心肌坏死(梗塞或瘢痕),前两种是可逆过程. 如果实行再血管化(revascularization)以后,恢复心肌血流,心肌细胞可以恢复功能. 后一种是不可逆损伤,