吡那地尔介导的超极化停搏液对未成熟兔心肌保护的研究

对20只幼兔随机分为吡那地尔介导的超极化停搏组（P组）和未加吡那地尔的去极化停搏组（S组）。通过改良的langendorff离体心脏灌流,观察两组心脏机械停搏时间、复跳时间、心肌收缩力、冠脉流量以及心肌中丙二醛（MDA）、乳酸脱氢酶（LDH）、肌酸磷酸激酶（CK）水平和心肌超微结构的变化。结果：P组心肌收缩力、冠脉流量恢复率均高于S组（P均〈0．05）,心肌LDH、MDA、CK水平较低（P均〈0．05）,心肌细胞超微结构较S组得到更好保护。认为吡那地尔介导的超极化停搏液对未成熟兔心肌的保护优于去极化停搏液。     

急性期脑卒中患者心肌酶与QT离散度的变化

目的探讨脑卒中患者急性期心肌酶、QT离散度的变化及意义。方法选择71例脑出血、78例脑梗塞患者和57例健康老年人，分别测定各组心肌酶、QT离散度，并进行比较。结果与对照组相比，脑出血组和脑梗塞组心肌酶显著升高、QT离散度明显延长（p〈0．01）；脑出血组和脑梗塞组比较，天冬氨酸转移酶（AST）、乳酸脱氢酶（LDH）、肌酸磷酸激酶（CK）显著升高（p〈0．01），肌酸磷酸激酶同工酶（CK—MB）、QT离散度（QTd）两组无显著性差异（p〉0．05）。结论脑卒中急性期心肌酶、QT离散度有显著变化，二者的监测有利于脑卒中病情及心脏受累程度的全面评价．对判断患者的预后有重要意义。     

20℃低温稀释血停搏液心肌保护效果的实验研究

目的：研究20℃低温稀释血停搏液（20℃HBC）灌注结合体循环自然降温在心脏直视手术中的心肌保护效果。方法：将14条15－20kg成年杂种犬随机分成对照组和实验组（n=7)，雌雄不拘，实验组采用间断20℃HBC灌注，体温自然降至32－35摄氏度，对照组采用体循环主动降温：间断8－10摄氏度稀释血停搏液（CBC）灌注。于主动脉阻断前、后抽取右房血测乳酸脱氢酶（LDH），肌酸激酶同工酶（CK－MB）、肌钙蛋白I（cTn-I)，取左心室心内膜下心肌观察超微结构变化，于主动脉阻断前、后监测心功能。结果：两组停搏液灌注后LDH，CK－MB,cTn-I均升高，实验组变化幅度小（P＜0．05）；实验组与对照组相比，灌注液对心功能影响较小，心肌超微结构损伤性变化不明显。结论：在体外循环过程中，与CBC相比，在心肌酶，cTn-I、心肌超微结构方面20℃HBC灌注对心肌有较好的保护作用。     

低硒与低营养复合因素致大鼠心肌损伤的实验研究

目的 探讨长期低硒与低营养复合因素膳食对大鼠心肌损伤的作用。方法 将Wistar大鼠40只随机分成2组，实验组用低硒、低蛋白、低维生素E饲料喂养，对照组用常硒、常蛋白、常维生素E饲料喂养，至第26周处死大鼠。测定全血谷胱甘肽过氧化物酶（GSH-Px）活性，血清肌酸激酶（CK）、肌酸激酶同工酶（CK-MB）、乳酸脱氢酶（LDH）水平和心脏质量与体质量比值。光镜、电镜下观察心肌结构改变。结果 实验组大鼠全血GSH墩活性水平显著低于对照组（t=58．79，P〈0．01）；实验组与对照组大鼠血清CK分别为（1．456±0．291）、（1．057±0．251）kU／L，CK—MB分别为（1．138±0．215）、（0．722±0．130）kU／L，LDH分别为（864．96±137．57）、（404．65±72．49）U／L，组间比较差异有统计学意义（t=4．71、7．46、13.42，P〈0．01）。大鼠心脏质量与体质量比值，实验组[（3．608±0．166）g／kg]显著高于对照组[（3．140±0．114）g／kg]，组间比较差异有统计学意义（t=10．62，P〈0．01）。光镜下实验组大鼠心肌出现散在小灶状坏死，检出率为66．67％，两组心肌病变检出率差异有统计学意义（χ^2=7．25，P〈0．01）。电镜下实验组大鼠部分心肌细胞线粒体嵴断裂，基质密度下降，细胞核固缩，早期凋亡形成，肌丝走行紊乱甚至溶解；对照组大鼠心肌细胞膜结构完好，线粒体嵴清晰，基质密度适中。结论 长期低硒、低营养复合因素膳食可引起大鼠心肌组织出现损伤。     

应用心肌梗死后72小时肌钙蛋白T浓度评估梗死范围

临床传统应用细胞酶 ,例如肌酸激酶 (CK )及其同功酶(CK MB)和乳酸脱氢酶 (LDH)来评估心肌细胞的损伤程度 ,但因其需要一系列测定来获得血清峰浓度或累积血清浓度而受到限制 ,此外 ,这些酶的表达不仅限于心肌 ,也使其特异性相对降低。与这些细胞标志物相反 ,肌钙蛋白T (TnT )是收缩组织的一种结构蛋白。急性心肌梗死 (AMI)后TnT会持续释放入血 ,其在血清中的浓度呈双相曲线。心肌梗死第 1日TnT由其细胞池释放进入循环形成第一峰 ,第 3～ 4日由于心肌蛋白降解又形成第二峰 ,与CK、CK MB和LDH等相比 ,TnT的第二峰几乎不受冠脉再灌…     

原发性甲减患者甲状腺功能与心肌酶谱的相关性研究

为探讨原发性甲状腺功能减退症(甲减)患者甲状腺功能与心肌酶谱的关系，检测了18例原发性甲减患者和18例查体健康者(对照组)的空腹血清游离三碘甲状腺原氨酸(FT3)、游离甲状腺素(FT4)、高敏促甲状腺(sTSH)、肌酸激酶(CK)及其同工酶CK—MB、乳酸脱氢酶(LDH)及其同工酶HBDH、天门冬酸氨基转移酶(AST)、总胆固醇(Tch)。结果显示，原发性甲减患者AST、CK、CK—MB、LDH、HBDH及Tch均明显高于对照组(P分别＜0．001、0．001、0．05、0．005、0．005、0．005)；sTSH和FT4与心肌诸酶、Tch均无相关性；FT3与CK—MB呈负相关(r＝-0．53，P＜0．05)，与Tch呈负相关(r＝-0．528，P＜0．05)。提示原发性甲减患者常伴心肌诸酶及Tch升高，其FT3水平下降与CK—MB、Tch升高关系更密切。     

ACS患者血清高敏C反应蛋白水平变化及意义

目的观察急性冠脉综合征（ACS）患者高敏c反应蛋白（hs．CRP）水平变化,并探讨其意义。方法采用酶联免疫吸附法检测60例ACS患者[不稳定型心绞痛32例（UAP组）,急性心肌梗死患者（AMI组）28例]和36例健康人（对照组）血清中的hs—CRP、血脂和心肌酶。结果血清hs．CRP水平UAP组、AMI组均显著高于对照组（P〈0．01）,AMI组高于UAP组（P〈0．05）;ACS患者hs—CRP水平与LDL-C呈正相关（r=0．460）,与HDL-C水平呈负相关（r=-0．350,P〈0．05）,与CK、CK-MB呈正相关（r分别为0．0．53、0．51,P〈0．05）。结论ACS患者血清hs-CRP升高,可作为诊断ACS及判断病情的指标。     

人参二醇组皂甙对大鼠心肌缺血再灌注损伤的保护作用

目的：探讨人参二醇组皂甙（PDS）对心肌缺血再灌注损伤的保护作用。方法：鼠心异位移植模型,移植心在4度缺血40min,86只Wistar老年大鼠分为3组,对照组（n=20),心脏用4度,St.Thomas冷晶心肌停搏液进行心肌保护,实验组（n=20)同对照组,但停搏液含PDS40mg/L,于移植心复跳30min,24h测心肌细胞内钙含量及血清中CK,CK－MB活力,空白组（n=6),阻断腹主动脉及下腔静脉40min,上述同时间测定CK,CK－MB活力,结果：PDS能降低心肌细胞内钙含量（P＜0．01）,降低血清中CK,CK－MB活力（P＜0．01）,结论：PDS作为St.Thomas心肌停博液的添加剂对心肌缺血再灌注损伤具有保护作用。     

肌钙蛋白T检测对急性心肌梗塞的诊断价值

对29例急性心肌梗塞（AMI）患者的肌钙蛋白T（TnT）和肌酸激酶（CK）等心肌酶谱进行监测，结果为：AMI后血清心肌TnT最早升高时间约在发病2h，升高幅度最大为正常临界值的55倍。发病5h内TnT阳性率为100％，而CK仅40％，前者显著高于后者。提示：TnT是一项特异性强、敏感性高的心肌损伤诊断指标，TnT升高可预示AMI患者心肌梗塞范围和心功能状况。     

复方黄精口服液对实验性大鼠心肌细胞自由基代谢及血清心肌酶的影响

目的：研究复方黄精口服液减轻阿霉素所致大鼠心脏毒性的作用及其机制。方法：通过腹可霉素复制大鼠实验性心力衰竭模型，测定心肌组织匀浆中超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH－Px)活性及血清心肌酶水平，并应用光镜电镜观察心肌组织的病理变化。结果：阿霉致鼠心力衰竭心肌组织SOD、GSH－Px活性降低，复方黄精口服液能逆转上述改变（P＜0．05）。复方黄精治疗组血清心肌酶肌酸激酶（CK）和乳酸脱氧酶（LDH）明显低于模型组（P＜0．05）。光镜、电镜结果显示：复方黄精治疗组心肌细胞损伤程度明显低于模型组（P＜0．05）。结论：复方黄精口服液具有抗自由基、降低心肌酶和保护心肌细胞超微结构的作用。     

Release kinetics of cardiac troponin T in coronary effluent from isolated rat hearts during hypoxia and reoxygenation

Summary A newly developed troponin T (TnT) test for the detection of myocardial cell necrosis has been reported to be very efficient in the detection of acute myocardial infarction. The aim of the present study was to determine whether cardiac TnT in coronary effluent from isolated heart perfused with albumin-free perfusion medium could be detected using the enzyme-linked immuno-sorbent assay developed by Katus et al. Isolated rat hearts were perfused according to the method of Langendorff. Coronary flow rate was measured by timed collection of the coronary perfusate that dripped from the hearts during 5 h of hypoxia (protocol A) or 4 h of hypoxia followed by 1 h of reoxygenation (protocol B). Creatine kinase (CK) and lactate dehydrogenase (LD) levels were compared with that of TnT. Myocardial adenine nucleotides were measured by HPLC. There was a strong correlation between TnT levels in albumin-free coronary effluent and TnT levels in coronary effluent diluted 1:1 with 5% bovine serum albumin (r=0.996, N=72). The coefficients of correlation between TnT and CK or LD during hypoxia and reoxygenation were 0.891 (N=88) and 0.871 (N=88), respectively. The coefficient of correlation between CK and LD was 0.993 (N=88). There were no significant differences in either the decrease of coronary flow or the increase of TnT content between the hearts in the two protocols. There was no significant correlation between TnT and energy charge of adenine nucleotides. These results indicate that cardiac TnT levels can be easily measured in albumin-free coronary effluent of isolated heart preparations. Like CK and LD, TnT is a good indicator for detecting myocardial cell damage. However, the release kinetics of TnT seem to be different than those of CK and LD. After 4 h of hypoxia, 1 h of reoxygenation has no effect on coronary flow rate or release of TnT. TnT did not determine energy charge at the end of hypoxia or reoxygenation.     

Effects of ischemic preconditioning on the release of cardiac troponin T in isolated rat hearts

Summary The aim of this study was to examine the effect of ischemic preconditioning on the releases of cardiac troponin T (TnT) during reperfusion in isolated rat hearts. Experiments were done on 22 rat hearts, which were perfused according to the method of Langendorff and were divided into the control group (n=14) and the preconditioning group (n=8). Double 5 min of ischemia each followed by 5 min reflow were applied as ischemic preconditioning. After 20 min of global ischemia, the releases of TnT, creatine kinase (CK), and lactate dehydrogenase (LD) in coronary effluent and the left ventricular developed pressure (LVP) were measured during 60 min of reperfusion. Ischemic preconditioning significantly suppressed the amounts of TnT released during reperfusion, as with those of CK and LD, and also improved contractile dysfunction (nine hearts in which ventricular fibrillation was sustained were excluded from the evaluation for hemodynamics), though the release kinetics of TnT was different from that of CK and LD. There were good inverse relationships between the LVP and the total amounts of TnT released during reperfusion period ( TnT) or TnT levels at 60 min of reperfusion. Cardiac TnT can be used as a useful biochemical marker for hemodynamics and myocardial damage after reperfusion.     

Myoglobin or enzymes for a rapid evaluation of infarction diagnosis?

Recently published clinical studies on patients with acute myocardial infarction (AMI) have documented that radioimmunologically determined serum peak concentrations of myoglobin (Mb) precede enzyme peak values. It has, therefore, been concluded that Mb (molecular weight 17,600) is liberated earlier from damaged myocardium than, for example, creatine kinase (CK, molecular weight 80,000). As rapid diagnosis is essential in the management of patients suffering from AMI, we have studied the liberation of cardiac enzymes and Mb using a nonrecirculating perfusion system. The release of malate dehydrogenase (MDH), lactate dehydrogenase (LDH), CK, and Mb from isolated guinea pig heart preparations was induced by anaerobic coronary perfusion at a constant flow rate. Thirty minutes after onset of anoxia there was a simultaneous increase in MDH, LDH, and Mb release. Maximum levels were reached between 120 and 180 min. The release curves for enzymes and Mb were approximately parallel. Close correlations exist between LDH/MDH (r = 0.94), CK/MDH (r = 0.98), LDH/Mb (r = 0.89), and MDH/Mb (r = 0.91). Based on these results and on calculations related to invasion and elimination kinetics, we suggest that the early peak of serum Mb in patients with AMI does not reflect a prior Mb release but depends on the more rapid rate of elimination of Mb from serum in comparison to enzymes.     

Release kinetics and correlation with hemodynamic dysfunction of cardiac troponin T in coronary effluent from isolated rat hearts during reperfusion

Summary Previously, we reported that cardiac troponin T (TnT) can be detected and measured in coronary effluent from isolated rat hearts during hypoxia. The present study was designed to evaluate the release kinetics of TnT from post-ischemic rat hearts. Using the Langendorff technique, the hearts were reperfused for 4h after 20 min or 60 min of global ischemia. Coronary flow was measured by timing the collection of the coronary perfusate that dripped from the hearts, and left ventricular pressure (LVP) was monitored continuously during the experiments. The amount of TnT released in 1 min was compared with the release of creatine kinase (CK) and lactate dehydrogenase (LD). The release kinetics of CK and LD showed a monophasic pattern and the levels at 4 h after reperfusion returned to baseline levels. By contrast, the release kinetics of TnT showed a small peak followed by a larger and more sustained peak. There were good negative correlations between developed pressure of LVP and both TnT and the amount of TnT released within 1 min at 4 h after reperfusion. These results indicate that the release kinetics of TnT is different from that of CK and LD during reperfusion, and further that cardiac TnT is a useful indicator of myocardial cell damage and can be used to evaluate the degree of myocardial cell damage in both the early and late phase of acute myocardial infarction.     

Myocardial contractile efficiency increases in proportion to a fetal enzyme shift in chronically infarcted rat hearts

Changes in creatine kinase (CK) and lactate dehydrogenase (LDH) isoform expression occur in residual tissue after myocardial infarction. It is unknown how these changes correlate with cardiac remodeling, contractile performance and efficiency. Rats were subjected to left coronary artery ligation (MI) or sham operation (sham). Left ventricular end–diastolic pressure (EDP) was measured in vivo 8 weeks later. Hearts were isolated, buffer–perfused (Langendorff) at constant pressure and isovolumetric left ventricular (LV) pressure–volume (PV) curves were recorded. LV PV areas (PVA) were calculated and related to oxygen consumption. Biopsies of intact left ventricular tissue were taken for biochemical measurements. Correlations between in vivo EDP and biochemical parameters were found: Total CK activity (r = –.47, p = .022), CK isoenzyme percentage for BB (r = +.57, p = .004), MB (r = +.54, p = .006) and CK–mito (r = –.51, p = .012), total creatine content (r = –.61, p = .002) and the ratio of LDH5/LDH1 (r = .49, p = .016). Correlations were also detected for left ventricular volume and PVAs at in vivo EDP demonstrating that the extent of CK and LDH system alterations correlate with the extent of LV dilatation and mechanical energy requirements. The slope of the MVO₂–PVA relation decreased significantly with increasing values of in vivo EDP (r = –.68, p = 0.0003) indicating increased contractile ef.ciency. Improved efficiency correlated with the increase in fetal CK isoenzyme expression. Thus, contractile efficiency increases parallel to the extent of left ventricular dilatation and dysfunction. CK and LDH system changes in residual intact myocardium also occur proportional to LV dysfunction.     

Prognostic significance of troponin T and MB creatine kinase elevations after percutaneous coronary interventions in patients with ischemic heart disease

AIM: To compare prognostic significance of troponin T (TnT) and MB creatine kinase (MB CK) elevations after percutaneous coronary interventions (PCI). MATERIAL AND METHODS: Patients with ischemic heart disease (n=122) were followed for 9+/-3 months after PCI. Coronary angiography was repeated in 79% of cases. Composite criterion of prognostic significance comprised coronary death or nonfatal myocardial infarction. RESULTS: Elevations of TnT , > or =0.03 ng/ml were noted in 55.5%, > or =0.1 ng/ml--in 21.9% of patients. Elevations of MB CK above upper limit of norm (ULN) were noted in 10.7% of patients. In 3 patients MB CK exceeded 3 ULN. Composite endpoint was registered in 53 patients (43.4%). There was no relation between any postprocedural elevation of MB CK and outcomes of follow-up. Levels of TnT between 0.03 and <0.1 hg/ml also were not related to prognosis. Post PCI TnT levels, > or =0.1 ng/ml were associated with significant worsening of prognosis during subsequent 6-12 months of follow-up.     

Late estimation of myocardial infarct size by total creatine kinase nomogram

We studied the possibility of enzymatic estimation of myocardial infarct size in patients late (between days 2 and 6) after the onset of acute myocardial infarction (AMI), in whom estimation of infarct size was difficult by analysis of time-activity curves of serum creatine kinase (CK) because of the lack of the enzymatic information during the initial 48 hours. Serial determinations of serum enzymes were performed in 32 patients within 6 hours after the onset of AMI and significantly close correlations were observed between cumulative total CK release and the cardiac fraction of lactate dehydrogenase isoenzyme (LDH1) activities from day 2 to day 6 after the onset of AMI (r = 0.863 to 0.870; p less than 0.001). We developed a nomogram to estimate cumulative total CK release by serum LDH1 activities obtained between days 2 and 6 after AMI and evaluated the reliability of the nomogram. Cumulative total CK release obtained from serial serum CK activities correlated closely with total CK release obtained from the nomogram in the second group of patients with AMI (r = 0.923 to 0.946; n = 24; p less than 0.001). Our total CK nomogram requiring few blood samples was useful in late estimation of infarct size in patients who were admitted to the hospital between days 2 and 6 after the onset of AMI.     

Troponin-T and brain natriuretic peptide as predictors for adriamycin-induced cardiomyopathy in rats.

BACKGROUND: Clinical methods for the early detection of doxorubicine (adriamycin; ADR) -induced cardiotoxicity have not been established. This study prospectively investigated whether atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and cardiac troponin T (TnT) are predictors for ADR-induced cardiotoxicity, and examined the correlations between the serum concentrations of these biomarkers and the functional alternations associated with ADR-induced myocardial damage. METHODS AND RESULTS: Male Wistar rats were injected weekly with 2 mg/kg of ADR via the tail vein for 8 weeks to induce cardiotoxicity. Echocardiograms of each ether anesthetized rat were taken at 6, 8, 10 and 12 weeks after the first administration of ADR, and blood samples collected from the tail vein were used to quantify plasma ANP and BNP, and serum TnT after echocardiography. Plasma BNP and serum TnT significantly increased from 6 to 12 weeks (81.5 to 173.3 pg/ml (p<0.001), <0.01 to 1.09 ng/ml (p<0.05), respectively) with deterioration of left ventricular % fractional shortening (%FS) (58.6% to 36.8%). The %FS significantly correlated with TnT (r=-0.51, p<0.001) and BNP (r=-0.75, p<0.0001); however, the increase of TnT was antecedent to the increase of BNP and the deterioration of %FS. CONCLUSION: Plasma BNP and serum TnT concentrations, especially TnT, measured by this highly sensitive method are useful predictors for ADR-induced cardiomyopathy.     

Impact of the revised criteria for acute myocardial infarction using cardiac troponins in a Japanese population with acute coronary syndromes.

BACKGROUND: The clinical implications of applying the new criteria of acute myocardial infarction (AMI) with cardiac troponins in terms of their diagnostic and prognostic impact in patients with suspected acute coronary syndromes (ACS) have not been well evaluated. METHODS AND RESULTS: The study group comprised 973 consecutive patients who were diagnosed as having ACS with or without ST elevation (STE). They were divided into 3 groups: unstable angina (UA) group (n=195) representing patients with no significant elevations of creatine kinase (CK) and troponin T (TnT); TnT-myocardial infarction (MI) group (n=170) with TnT elevation and no CK elevation (additionally detected AMI by the new criteria); CK-MI group (n=608) with significant elevation of CK (AMI by the old criteria). In the TnT-MI group, 140 (76%) patients had non-STE ACS. In-hospital mortality rates for STE ACS were 0%, 2.5% and 9.7% in the UA, TnT-MI and CK-MI groups, respectively. The corresponding values for non-STE ACS were 1.8%, 4.6%, and 16.5%, respectively (p<0.0001), suggesting a pivotal role of TnT. In multiple logistic regression analysis, significant CK elevation was selected as an independent predictor of in-hospital death in concurrence with age > or =75 years, prior MI, shock and low left ventricular ejection fraction in non-STE ACS. CONCLUSIONS: The new criteria result in a substantial increase in the diagnosis of AMI from non-STE ACS in particular. They assist greatly in detailed risk stratification of ACS patients, notably in cooperation with the old CK criteria.