缬沙坦加参麦注射液治疗充血性心力衰竭的临床观察

目的观察缬沙坦（Valsartan）加参麦注射液（Shenmai Injection,SI）对充血性心力衰竭（CHF）心肌损害的疗效。方法采用随机分组的方法,分别用常规治疗（31例）和缬沙坦、SI加常规治疗（31例）,并对CHF的各项实验室指标[血浆肌钙蛋白T（cTnT）、心肌酶谱]进行观察。结果在CHF进程中,cTnT浓度随着心功能恶化呈进行性增高。应用缬沙坦加SI治疗2周后,患者左室收缩功能得到明显改善,未发现严重不良反应。结论血浆cTnT可作为CHF患者预后判断的一项重要生化指标。缬沙坦加SI是治疗CHF安全有效的药物。     

肌钙蛋白T在诊断急性心肌梗死中的应用

采用肌钙蛋白Ｔ半定量试纸条检测急性心肌梗死１６例，心绞痛１３例，以２０例健康体检者为对照组。结果显示，ＡＭＩ组阳性反应１５例，心绞组仅１例阳性，对照组均为阴性，结果提示，ＴｎＴ半定量试纸条检测法在ＡＭＩ诊断中，敏感性和特异性较高，方法简便方便，尤其适用于急诊室，内科监护病房及基层医院使用。     

用金标法快速测定血清中cTn-Ⅰ在急性心肌梗死诊断上的应用

为探讨急性心肌梗死和疑为心梗病人血中 c Tn I的敏感性和特异性 ,采用金标法对 5 2例就诊病人测定其血中 c Tn- 和酶学法测定 CK- MB两个指标 ,结果发现急性心肌梗死组病人血中的 c Tn- 敏感度高于 CK- MB,但二者无显著性差异 ;而疑为心梗病人血中的 c Tn- 敏感度高于 CK- MB且具有显著的特异性。c Tn- 的测定对急性心肌梗死病人的诊断和治疗具有特别重要的意义     

病毒性心肌炎心肌肌钙蛋白Ⅰ检测的临床意义

目的:对病毒性心肌炎患儿血中肌钙蛋白I(cTn I)含量进行检测,探讨与临床的关系。方法:采用放射免疫法对24例病毒性心肌炎患儿血中cTn I进行定量检测,同时检测血清心肌酶谱的改变情况,并就两种指标进行相关性探讨。结果:病毒性心肌炎患儿血中cTn I含量明显增高(4.5±2.2 )vs(2.3±0.3)ng/ml,P<0.01),并与CKMB,LDH_1的含量呈明显的正相关。结论:cTnl I是诊断病毒性心肌炎的敏感指标,可以反映出心肌受损的程度。     

人心肌肌钙蛋白T的提取、纯化及鉴定研究

目的 :探究一种简便易行的人心肌肌钙蛋白T(cTnT)的提纯方法并进行鉴定。　方法 :采用匀浆、离心、70℃加热、冰浴、饱和硫酸铵盐析、透析、DEAE 纤维素层析等方法提纯cTnT ,并进行鉴定和免疫活性检测。　结果 :1 0 0g心肌组织中获得cTnT 2 1 .35 6mg ,纯度最高达 91 .7%。　结论 :建立的方法能成功提取纯度较高 ,且具有免疫活性的人心肌cTnT ,为建立适用于临床的cTnT检测方法奠定基础     

Induction of specific anti-actin antibodies and their measurement by ELISA technique.

Using the ELISA technique we have been able to quantify antibodies directed against actin and to follow the kinetics of antibody production. Specific anti-actin antisera have been raised in rabbits by immunization with chemically modified white muscle rabbit actin. Two or three dinitrophenyl groups linked per actin molecule were sufficient to break natural tolerance, while linkage of three phosphorylcholine groups to actin was not.     

不同给药途径的腺苷预处理对大鼠缺血再灌注心肌的保护

Objective To evaluate the effect on myocardial protection of adenosine preconditioning in different route of administration through right jugular vein and left ventricle.Methods 48 SD rats were randomly divided into ischemia reperfusion group(blank control),ischemic preconditioning group(IP,positive control),adenosine venous infusion group,adenosine in ventricular group,normal saline(NS)venous infusion group(negative control I)and NS in ventricular group(negative control Ⅱ).The ischemia reperfusion rats model were established in vivo,and then changes of heart function,serum cardiac troponin T (cTnT),superoxide dismutase(SOD),malondialdehyde(MDA)and expression of nuclear factor KB(NF-kB) were observed.Results SOD in IP[(208.63±23.88)U/ml],adenosine venous infusion group [(178.27±11.56) U/ml]and adenosine in ventricular group[(191.31±28.14)U/ml]were significantly higher than that in the ischemia reperfusion group[(145.05±23.18)U/ml](P<0.05),cTnT,MDA and expression of NF-kB were lower than that in the ischemia reperfusion group (P<0.05).Heart function was significantly better than that in the ischemia reperfusion group(P<0.05);SOD in adenosine in ventricular group was significantly higher than that in adenosine venous infusion group(P<0.05).cTnT,MDA and expression of NF-kB were lower than that in adenosine venous infusion group (P<0.05).Conclusion Adenosine preconditioning may mimic protective effect of ischemic preconditioning. The effect on myocardial protection of adenosine in ventricular group was better than that of adenosine venous infusion group.     

不同给药途径的腺苷预处理对大鼠缺血再灌注心肌的保护

Objective To evaluate the effect on myocardial protection of adenosine preconditioning in different route of administration through right jugular vein and left ventricle.Methods 48 SD rats were randomly divided into ischemia reperfusion group(blank control),ischemic preconditioning group(IP,positive control),adenosine venous infusion group,adenosine in ventricular group,normal saline(NS)venous infusion group(negative control I)and NS in ventricular group(negative control Ⅱ).The ischemia reperfusion rats model were established in vivo,and then changes of heart function,serum cardiac troponin T (cTnT),superoxide dismutase(SOD),malondialdehyde(MDA)and expression of nuclear factor KB(NF-kB) were observed.Results SOD in IP[(208.63±23.88)U/ml],adenosine venous infusion group [(178.27±11.56) U/ml]and adenosine in ventricular group[(191.31±28.14)U/ml]were significantly higher than that in the ischemia reperfusion group[(145.05±23.18)U/ml](P<0.05),cTnT,MDA and expression of NF-kB were lower than that in the ischemia reperfusion group (P<0.05).Heart function was significantly better than that in the ischemia reperfusion group(P<0.05);SOD in adenosine in ventricular group was significantly higher than that in adenosine venous infusion group(P<0.05).cTnT,MDA and expression of NF-kB were lower than that in adenosine venous infusion group (P<0.05).Conclusion Adenosine preconditioning may mimic protective effect of ischemic preconditioning. The effect on myocardial protection of adenosine in ventricular group was better than that of adenosine venous infusion group.     

Cardiac drift during prolonged exercise with echocardiographic evidence of reduced diastolic function of the heart

This study examined whether, in 16 male subjects, a continuous increase in heart rate (HR) during 4 h of ergometry cycling relates to cardiac fatigue or cardiomyocyte damage. Serum cardiac troponin T (cTnT) was determined and echocardiographic assessment was carried out prior to and after 2 h of exercise, within 15 min of completing exercise and after 24 h. Left ventricular contractile function (end-systolic blood pressure–volume relationship [SBP/ESV]) and diastolic filling (ratio of early to late peak left ventricular filling velocities [E:A]) were calculated. During exercise HR was 132±5 beats min^–1 after 2 h and increased to 141±5 beats min^–1 (mean ± SD; P<0.05), but there was no evidence of altered LV contractile function (SBP/ESV 39.0±5.1 mmHg cm^–1 to 36.5±5.2 mmHg cm^–1 and SBP/ESV was not correlated to maximal oxygen uptake (r²=0.363). In contrast, E:A decreased (1.82±0.32 to 1.48±0.30; P<0.05) and returned towards baseline after 24 h (1.78±0.28), and individual changes were correlated to maximal oxygen uptake (r²=0.61; P<0.05). Low levels of cTnT were detected in two subjects after 4 h of exercise that had normalised by 24 h of recovery. During prolonged exercise cardiovascular drift occurred with echocardiographic signs of a reduced diastolic function of the heart, especially in those subjects with a high maximal oxygen uptake.