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心肌损伤指标
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  myocardial injury markers
     Objective To evaluate the clinical diagnostic value of myocardial injury markers such as cardiac troponin T , troponin I and conventional myocardial enzyme in acute viral myocarditis.
     目的 探讨心肌损伤指标肌钙蛋白T(cTnT)、肌钙蛋白I(cTnI)对急性病毒性心肌炎的临床诊断价值。
短句来源
     Conclusion As myocardial injury markers serum cTnT and cTnl are more sensitive than conventional CK,CK-MB,sGOT,LDH for acute phase of patients with viral myocarditis. They are good observatory markers which can respond myocardiac injury timely.
     结论 病毒性心肌炎患者在急性期心肌损伤指标检测中,cTnT、cTnI比传统的CK、CK-MB、sGOT、LDH有更好的敏感度,是及时反映心肌损伤的良好的观察指标。
短句来源
     The plasma myocardial injury markers CK-MB and cTnI were measured at the four points: ①After induction; ②1 hour after coronary anastomosis; ③ 6 hours and ④ 24 hours after the operation.
     测量麻醉诱导后、冠状动脉血管吻合后 1h、术后 6h以及术后 2 4h各时间点肺动脉血中心肌损伤指标肌酸激酶同工酶 (CK MB)和肌钙蛋白Ⅰ (cTnI) ;
短句来源
     Result Myocardial injury markers CK-MB and cTnI increased significantly after the anastomosis in each group; cTnI was lower in the aprotinin group than in the control group at the third and forth points(P<0.05).
     结果 CK MB和cTnI在两组内于吻合后均明显升高 ,抑肽酶组心肌损伤指标cTnI在术后 6h和 2 4h均低于对照组 (P <0 0 5 ) ;
短句来源
  myocardial damage markers
     The Relationship among Left Ventricular Diastolic Function and Serum Myocardial Damage Markers,Etiology,Electrocardiography in Adult Mild Viral Myocarditis
     成人轻症病毒性心肌炎左室舒张功能与血清心肌损伤指标、病原学、心电图表现的关系
短句来源
  myocardiac injury marker
     Objective:To evaluate the clinical significance of non-specific cell inflammatory factor tumor necrosis factor α (TNF-α) and myocardiac injury marker troponin T(cTnT) on those patients with acute viral myocarditis.
     目的 :探讨心肌损伤指标肌钙蛋白T(cTnT)与非特异细胞炎症因子肿瘤坏死因子 α(TNF α)在急性病毒性心肌炎 (VMC)患者中检测的临床意义。
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  “心肌损伤指标”译为未确定词的双语例句
     Clinical diagnoses mainly rely on virus infection history,clinical symptoms and indexes of cardiac injury.
     结论临床症状和体征无特异性,临床诊断主要依赖于病毒感染史、临床症状、心肌损伤指标;
短句来源
     Multiple regression analysis indicated that peak CK and CK-MB were only related with the striated muscular injury and were not affected by the indexes of the myocardial injury(ECG and CTnI);
     多元回归分析显示,CK及CK-MB峰值均只与横纹肌损伤相关,而不受心肌损伤指标(ECG、CTnI)的影响;
短句来源
     Results The levels of AST, LDH, CK, CK-MB in the TMP group were lower than those in the control group(P<0.05).
     结果两组主动脉阻断时间比较差异无统计学意义。 CPB期间两组患者心肌损伤指标AST、LDH、CK、CK-MB明显升高(P<0.05),川芎嗪组心肌酶含量明显低于对照组(P<0.05)。
短句来源
     Objective To evaluate the sensitivity and specificity of cardiac Troponin T(cTnT) as a marker of myocardial injury.
     目的 评价心肌肌钙蛋白T(cTnT)作为判断心肌损伤指标的敏感性和特异性。
短句来源
     Objective: To evaluate the value of serum cardiac troponin I(cTnI)as a marker in diagnosing acute myocardial infarction(AMI),unstable angina pectoris(AP)and acute virual m yocarditis(AVM).
     目的:探讨心肌肌钙蛋白I(cTnI)作为一种心肌损伤指标对急性心肌梗死(AMI)、不稳定型心绞痛(UA)及急性病毒性心肌炎(AVM)的诊断价值。
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  myocardial injury markers
Patients present with typical chest pain, ECG changes suggesting ischemia, and a slight elevation of myocardial injury markers such as Creatine kinase and Troponines.
      
An increase in myocardial injury markers are also similar and have the same prognostic meaning as in men.
      


The contents of serum cardiac specific troponin T (cTnT) and creatine kinase isoenzyme MB (CK-MB) aetivity were measured by enzyme immunoassay method in 42 patients with stable angina (SA ) and 86 patients with unstable angina (UA ) every four hours for 48 hours after admission to the hospital. The outcomes of interest during the hospitalization were acute myocardiol infarction (AMI) and sudden death. Results: cTnTn was detected (range, 0. 20~ 1. 86 μg per liter; mean 0. 98; median, 0. 17 ) in the serum of 28...

The contents of serum cardiac specific troponin T (cTnT) and creatine kinase isoenzyme MB (CK-MB) aetivity were measured by enzyme immunoassay method in 42 patients with stable angina (SA ) and 86 patients with unstable angina (UA ) every four hours for 48 hours after admission to the hospital. The outcomes of interest during the hospitalization were acute myocardiol infarction (AMI) and sudden death. Results: cTnTn was detected (range, 0. 20~ 1. 86 μg per liter; mean 0. 98; median, 0. 17 ) in the serum of 28 of the 86 patients (32. 6 percent ) with UA.Only two of these patients had elevated CK-MB (one was positive for cTnT, the other was negative). of the 28 patients who were positive for cTnT, 7 cases had AMI and 1 case had sudden death within one week after admission. In contrast only one of the 58 patients with UA who were negative for cTnT developed AMI (P<0.001),none had sudden death. cTnT was not detected in any of the 42 patients with SA, and none of these patients died in the same time. Conclusion: ①cTnT in serum appears to be a more sensitive and specifie indicator of mycardial cell injury than serum CK-MB; ② the elevating cTnT in serum of UA patient may probably indicate that the patient has already had a miero-infarction or none Q-infarction; ③ positive cTnT may be a prognostic indicator for unfavorable outcome to UA palients; ④ the patient who is negalive for cTnT may have a good outcome.

为探讨心脏特异性肌钙蛋白T(cTnT)在不稳定性心绞痛(UA)患者血清中检测的临床意义。应用酶联免疫法测定42例稳定性心绞痛(SA)患者和86例UA患者血清cTnT、肌酸磷酸激酶同功酶-MB(CK-MB).并作对照分析。结果显示:SA患者血清cTnT无例升高(以cTnT>0.2μg/L为界限值);28例UA患者血消cTnT至少有1次升高.占32.6%,先均值为0.98±0.47μg/L,范围为0.20~1.86μg/L,这28例在入院后1周内有7例发生急性心肌梗塞(AMI),1例发生猝死;其余58例。cTnT不升高者中,在相同时间内,仅1例发生AMI,无猝死者。UA患者中cTnT阳性与阴性者的预后差别有统计意义(χ2=14.26,P<0.001)。UA中CK-MB只有2例轻度升高,其中cTnT阳性与阴性各占1例。结果提示:①cTnT为较CK-MB更敏感、更特异的反应心肌损伤的指标;②UA中约有32.6%的患者血清cTnT异常升高,说明这部分患者已经发生心肌细胞损伤、心内膜下心肌梗塞或小灶性心肌梗塞,该类患者处于高危状态,极易发展成典型的AMI或猝死;③UA中cTnT不升高者,在很大程度上将有一个良好的预后。

Mitogen activated protein kinase (MAPK) is involved in the delayed protection (DP) of preconditioning (PC). MAPK activities in myocardium or cultured cardiomyocytes were assayed at the 0h, 12h, and 24h after PC on the model of rabbit heart in situ or the cultured cardiomyocytes. The myocardial infarct size, LDH release, cell viability, and the content of cellular MDA were measured with or without the intervention of PD 098059, the inhibitor of MAPK, in the models before PC and different time intervals after...

Mitogen activated protein kinase (MAPK) is involved in the delayed protection (DP) of preconditioning (PC). MAPK activities in myocardium or cultured cardiomyocytes were assayed at the 0h, 12h, and 24h after PC on the model of rabbit heart in situ or the cultured cardiomyocytes. The myocardial infarct size, LDH release, cell viability, and the content of cellular MDA were measured with or without the intervention of PD 098059, the inhibitor of MAPK, in the models before PC and different time intervals after PC. Results showed that the MAPK activities were increased significantly immediately after PC ( P <0.01) and decreased to control level at 12h and 24h after PC ( P >0.05) compared with those in normal group. The infarct sizes and the rise of plasma LDH level were greatly decreased in preconditioned myocardium after a long time ischemia/reperfusion (I/R) than those in the unpreconditioned. Compared with the cardiomyocytes unconditioned, the number of viable cell (71.0±1.6 vs 48.2±2.2%, P <0.01) was greatly increased, the cellular MDA contents (33.5±12.8 vs 103.5± 15.0 nmol/mg Pr., P <0.01) and the LDH release (850.0±139.1 vs 1552.0±102.6 IU/L, P <0.01) were dramatically decreased in preconditioned ones. The inhibition of MT′s production with PD 098059 completely removed all the delayed protection at 24h after PC. Conclusion: The myocardium or cardiomyocytes at 24h after PC are offered more capacity to tolerate the I/R damage, and MAPK is involved in the delayed protection.

为探讨丝裂素活化蛋白激酶(mitogen-activatedproteinkinase,MAPK)参与心肌缺血预适应的延迟保护作用。我们在原位兔心脏缺血预适应和培养乳兔心肌细胞缺氧预适应的模型上,检测预适应后即刻、12小时和24小时MAPK活性变化,观察预适应后24小时对再次长时间缺血/再灌注或缺氧/复氧损伤的保护作用(心肌梗塞范围、细胞存活率、LDH释放和细胞MDA含量),以及用特异的MAPK系统抑制剂PD098059抑制预适应后MAPK活性的增高对预适应后延迟保护作用的影响。结果提示:MAPK活性在预适应后即刻增高10倍以上(P<0.01),在12小时和24小时降至或接近正常对照水平。与未预适应的心肌组织或心肌细胞遭受缺血/再灌注或缺氧/复氧的损伤相比较,预适应后24小时其心梗范围缩小,血浆LDH活性升高程度减轻,心肌细胞存活率增高,细胞MDA含量和LDH释放均降低(均P<0.01)。用PD098059抑制MAPK活性增高时,则消除了预适应后的延迟保护作用,上述心肌损伤指标接近单纯缺血/再灌注组或缺氧/复氧组(P>0.05)。结论:(1)预适应后24小时心肌或心肌细胞对再次缺血/再灌注或缺氧/...

为探讨丝裂素活化蛋白激酶(mitogen-activatedproteinkinase,MAPK)参与心肌缺血预适应的延迟保护作用。我们在原位兔心脏缺血预适应和培养乳兔心肌细胞缺氧预适应的模型上,检测预适应后即刻、12小时和24小时MAPK活性变化,观察预适应后24小时对再次长时间缺血/再灌注或缺氧/复氧损伤的保护作用(心肌梗塞范围、细胞存活率、LDH释放和细胞MDA含量),以及用特异的MAPK系统抑制剂PD098059抑制预适应后MAPK活性的增高对预适应后延迟保护作用的影响。结果提示:MAPK活性在预适应后即刻增高10倍以上(P<0.01),在12小时和24小时降至或接近正常对照水平。与未预适应的心肌组织或心肌细胞遭受缺血/再灌注或缺氧/复氧的损伤相比较,预适应后24小时其心梗范围缩小,血浆LDH活性升高程度减轻,心肌细胞存活率增高,细胞MDA含量和LDH释放均降低(均P<0.01)。用PD098059抑制MAPK活性增高时,则消除了预适应后的延迟保护作用,上述心肌损伤指标接近单纯缺血/再灌注组或缺氧/复氧组(P>0.05)。结论:(1)预适应后24小时心肌或心肌细胞对再次缺血/再灌注或缺氧/复氧的损伤?

Objective To stady whetter metallothionein (MT) is an OH scanvenger and plays a protective role in cardiac ischemic/reperfusion injury. MT involves in the delayed protection 24 hr after preconditioning (PC). Methods MT contents in myocardium or cultured cardiomyocytes are assayed at the 0 hr, 12hr, and 24 hr after PC on the model of rabbit heart in situ or that of the cultured cardiomyocytes. The myocardial infarct size, LDH release, cell viability, and the content of cellular MDA were measured with...

Objective To stady whetter metallothionein (MT) is an OH scanvenger and plays a protective role in cardiac ischemic/reperfusion injury. MT involves in the delayed protection 24 hr after preconditioning (PC). Methods MT contents in myocardium or cultured cardiomyocytes are assayed at the 0 hr, 12hr, and 24 hr after PC on the model of rabbit heart in situ or that of the cultured cardiomyocytes. The myocardial infarct size, LDH release, cell viability, and the content of cellular MDA were measured with or without the intervention of PD 098059 , the inhibitor of mitogen activated protein kinase in the models before PC and different time intervals after PC. Results The MT contents were increased significantly at 12 hr(1406 2±112 2vs 129 9±10 4pmol/mg Pr., P <0 01, in cardiomyocytes )and 24hr (1032.7±199.1vs 129.9±10.4pmol/mg Pr., P <0.01, in cardiomyocytes; 62.1±12.6vs 27.2±3.7pmol/mg Pr., P <0.01, in myocardium) after PC compared with those in normal group. The infarct sizes (13.2 ±3.6% vs 32.3±5.7%, P <0.05) and the rise of LDH release in plasma (1944±256vs 2826±239IU/L, P <0.05) were greatly decreased in preconditioned myocardium after a long time ischemia reperfusion than those in the unpreconditioned. Compared with the cardiomyocytes unconditioned, the number of viable cell (71.0±1.6 vs 48.2±2.2%, P <0.01) was greatly increased, the cellular MDA contents (33.5±12.8 vs 103.5±15.0nmol/mg Pr., P <0.01) and the LDH release (850.0±139.1 vs 1552.0±102.6 IU/L, P <0.01) were dramatically decreased in preconditioned ones. All the delayed protection at 24 hr after PC were completely disappeared with the inhibition of 作者单位:100034 北京医科大学第一医院(陈 魁、张钧华、陈 ? ⒄耪窀铡⑼衾鲛?,北京医科大学心血管基础研究所(叶 赤、刘秀华、庞永政、唐朝枢) MT′s production with PD 098059 ( P >0.05). Conclusion The myocardium or cardiomyocytes at 24 hr after PC are offered more capacity to tolerate the I/R damage, and MT involves in the delayed protection.

探讨金属硫蛋白(MT)参与心肌缺血预处理延迟保护作用的可能性。方法在原位兔心脏缺血预处理和培养乳兔心肌细胞缺氧预处理的模型上,检测预处理后即刻,12小时和24小时MT含量的变化,观察预处理后24小时对再次长时间缺血-再灌注或缺氧-复氧损伤的保护作用以及用丝裂素蛋白激酶抑制剂PD098059抑制预处理后MT含量增高对预处理后延迟保护作用的影响。结果MT含量在预处理后12小时(心肌细胞)和24小时(心肌细胞和心肌组织)显著增高,与未预处理的损伤的心肌组织或心肌细胞相比较,预处理后24小时其心肌梗塞范围缩小,血浆乳酸脱氢酶活性升高程度减轻,心肌细胞存活率增高,细胞丙二醛含量和乳酸脱氢酶释放均降低。用PD098059抑制MT生成时,则消除了预处理后的延迟保护作用,上述心肌损伤指标接近缺血-再灌注组或缺氧-复氧组(P>0.05)。结论预处理后24小时心肌或心肌细胞对再次缺血-再灌注或缺氧-复氧的损伤有保护作用。MT参入心肌或心肌细胞预处理后的延迟保护作用。

 
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