2型糖尿病大鼠早期血清cTnI水平与心功能的变化

目的:研究2型糖尿病大鼠早期血清心肌肌钙蛋白I(cTnI)的水平及心功能变化,探讨早期2型糖尿病大鼠血清cTnI水平与糖尿病心肌损伤发生发展之间的关系,明确cTnI在糖尿病心肌病发生发展中的作用。方法:通过高脂饮食联合链脲佐菌素建立2型糖尿病大鼠模型,实验将大鼠分为正常对照组、糖尿病2周模型组及4周模型组,超声心动图检测心功能相关指标,血清检测空腹血糖(FBG)、总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白(HDL-C)、低密度脂蛋白(LDL-C)、空腹胰岛素(FINS)及cTnI水平,HE染色法观察心肌病理结构变化,Western blot法检测心肌cTnI蛋白表达变化,通过上述指标变化分析2型糖尿病大鼠早期血清cTnI与大鼠心功能改变之间的关系。结果:与正常组比较,2型糖尿病大鼠TC、TG、LDL-C水平显著升高,HDL-C水平显著降低;糖尿病大鼠4周模型组与2周模型组相比较,TC、TG、LDL-C水平升高更明显,HDL-C水平降低更显著(P0.01);显微镜下糖尿病组大鼠心肌可见局灶性心肌细胞变性、坏死;糖尿病组大鼠相对于正常对照组血清及心肌cTnI表达显著增加(P0.01),且4周模型组比2周模型组增加更明显。结论:糖尿病大鼠早期即出现cTnI水平升高和心功能改变,有望为糖尿病心肌病的早期诊断和治疗提供理论依据。     

实验性心肌缺血内皮素的动态变化

目的:观察心肌缺血对血浆及心肌组织内皮素(ET)浓度影响的量效及时效改变,并初步探讨其机制。方法:用不同剂量的垂体后叶素(Pit)诱发大鼠在体心肌缺血并观察了相同剂量Pit作用下的不同时点的大鼠心肌组织及血浆的ET浓度的变化,然后做心肌ET-1的免疫组化及基因表达。结果:随着Pit剂量的加大,血浆及心肌组织ET浓度逐渐升高,当Pit剂量升至15U/kg体重时,其ET浓度高于对照组(P＜0.05);Pit注射后1hET浓度升至高峰,当缺血时间大于1h后,ET浓度有所回降,但仍明显高于对照组。免疫组化显示ET-1主要定位在心肌细胞和血管内皮细胞,缺血组心肌ET-1染色灰度值明显低于对照组(P＜0.01);RT-PCR结果显示缺血组PCR产物条带灰度值显著高于对照组(P＜0.01)。结论:垂体后叶素性心肌缺血可引起血浆及心肌ET浓度的升高并呈现一定的量效及时效关系,这可能与缺血刺激心肌ET-1基因的表达及蛋白合成有关。     

烫伤大鼠脑底动脉ET-1水平的测定及意义

目的:探讨烫(烧)伤损伤对大鼠脑血管内皮素-1(Endothelin-1,ET-1)表达的影响,探讨内皮素-1在大鼠烫(烧)伤损伤诱发脑血管痉挛致脑功能障碍的作用。方法:Wistar大鼠随机分为单纯烫伤组(单烫组)、烫伤合并注射内毒素组(烫注组)、单纯注射内毒素组(单注组)三大组。各组再分为正常对照组、3h组、6h组、12h组、24h组、48h组,应用放射免疫分析测定(radioimmunoassay),分别检测各组实验动物脑基底动脉ET-1水平的变化。结果:单烫组、烫注组和单注组各组损伤后大鼠脑基底动脉ET-1水平较正常对照组增高,6h达高峰,12h仍持续较高水平。结论:烫(烧)伤损伤可引起大鼠脑血管ET-1显著增加,增加的ET-1在烫(烧)伤损伤诱发脑血管痉挛、引发脑血液循环障碍的病理发生过程中可能起重要作用。     

川芎嗪对腹主动脉缩窄大鼠血浆内皮素-1水平的影响

目的:探讨川芎嗪对腹主动脉缩窄大鼠血浆内皮素(endothelin-1,ET-1)水平的干预作用。方法:实验大鼠随机分为假手术组、模型组和川芎嗪组。银夹法建立腹主动脉缩窄大鼠模型,川芎嗪组用25mg/kg川芎嗪注射液,余两组用等量双蒸水(1.5ml/100g)灌胃4周后,比较各组血浆ET-1浓度、大鼠左室心肌质量指数(LVMI)和左室心肌病理形态胶原染色等的变化。结果:模型组LVMI、血浆ET-1浓度和心肌胶原纤维化较假手术组显著升高(P0.01),川芎嗪组较模型组显著降低(P0.01)。结论:川芎嗪可防治腹主动脉缩窄大鼠心肌纤维化,可能与影响血浆ET-1水平有关。     

川崎病并发冠脉病变患儿血浆ET-1和血清Hcy、cTnI检测的临床意义

目的:探讨了川崎病并发冠脉病变患儿血浆ET-1和血清Hcy、cTnI检测的变化及临床意义。方法:应用放免法、免疫结合和生化法对31例川崎病并发冠脉病变患儿进行了血浆ET-1和血清Hcy、cTnI测定,并与35例正常儿童作比较。结果:川崎病并发冠脉病变患儿血浆ET-1和血清Hcy、cTnI水平均显著地高于正常儿组(P<0.01),且血浆ET-1和血清Hcy、cTnI水平呈正相关(r=0.4782、0.5014,P<0.01)。结论:检测川崎病并发冠脉病变患儿血浆ET-1和血清Hcy、cTnI水平的变化对疾病的发生和发展及预后均有重要的临床价值。     

电磁辐射对清醒大鼠动脉收缩压的影响及其机制研究

目的:观察电磁辐射(EMR)对大鼠整体血压的影响并初步探讨其机理。方法:用无创性的尾套式大鼠动脉血压测量仪观察一定场强和脉冲次数的EMR照后不同时间内清醒大鼠动脉收缩压的变化规律,并观察血液中前列环素(PGI2)、血栓烷素(TXA2)、内皮素(ET),心钠素(ANP)、一氧化氮浓度及一氧化氮合酶活性的变化。结果:照射后的大鼠的动脉血压先升高,维持至第2 h,开始下降,在第12 h下降至最低点,而后开始缓慢回升,在到第24 h,逐渐恢复接近正常水平。在收缩压变动的最显著的第12 h,血浆前列腺环素和心钠素的浓度明显降低,内皮素含量升高,血栓素在照射后没有显著改变,NOS活性升高,NO含量略有升高,但无显著差异。结论:EMR照射后,大鼠血压呈规律性改变,内皮素、心钠素、前列环素参与了辐射引起的血压波动,NO/NOS系统在其中的作用尚不能肯定。     

心房钠尿肽对脂多糖所致大鼠急性肺损伤的影响

目的:探讨心房钠尿肽(ANP)对脂多糖(LPS)血症大鼠急性肺损伤的作用和机制。方法: 大鼠静脉给予LPS(2 mg·kg^－1)后立即静脉给予ANP(2 μg·kg^－1),记录动物平均动脉血压(MAP)、检测血浆一氧化氮(NO)和内皮素(ET)浓度、测定肺水含量并做肺组织病理学检查。结果: 给予LPS的大鼠,MAP持续下降,至4 h MAP(8.1±2.6)kPa;血浆NO和ET浓度均显著升高(P<0.01 vs control);4 h肺湿干比(5.15±0.43),显著高于对照组(P<0.05);大鼠肺组织病理学检查呈现肺间质水肿。LPS＋ANP组大鼠MAP在给药初期的短暂下降后逐步回升,至4h MAP(13.4±2.9)kPa(P<0.05 vs LPS);4 h血浆NO水平和ET浓度均显著下降(P<0.05 vs LPS),但仍明显高于对照组(P<0.01 vs control);肺湿干比(4.57±0.35)与对照组没有显著差异;肺组织病理学改变较LPS组明显减轻。结论: ANP对LPS引起的急性肺损伤有治疗作用,能调节LPS引起的动脉血压的持续下降,上述作用可能与ANP拮抗ET的产生、降低NO的分泌有关。     

内毒素血症大鼠脑底动脉内皮素-1能神经纤维表达与分布的变化

目的:探讨内毒素血症大鼠脑底动脉内皮素-1(ET-1)能神经纤维诱发脑血管痉挛发生与发展的关系,为深入阐明内毒素血症诱发脑血管痉挛的发病机制提供形态学依据。方法:96只Wistar大鼠随机分为对照组、内毒素血症组(注射内毒素第3、6、12、24、48h),分别采用放射免疫法检测血浆内皮素-1水平的变化,采用免疫组织化学ABC法对大鼠脑底动脉内皮素-1能神经纤维进行观察。结果:内毒素血症后3、6、12h大鼠血浆内皮素-1水平较对照组明显升高(P0.05),内毒素血症后24h和48h已趋于正常(P0.05)。此外,对照组和内毒素组大鼠脑底动脉可见棕褐色,呈细线状分布的内皮素-1能免疫反应阳性纤维,其中内毒素血症后第6h和12h大鼠脑底动脉内皮素-1能神经纤维密度显著增高(P0.05)。结论:内毒素血症大鼠血浆内皮素-1水平升高,脑底动脉内皮素-1能神经纤维密度增加,提示内皮素-1参与了内毒素血症诱发脑血管痉挛的病理生理过程,为脑血管痉挛的神经-体液调节机制提出了新思路,同时为临床预防和治疗脑血管痉挛提供了理论依据。     

电烧伤大鼠创面组织中VEGF及血清ET-1表达水平的变化

目的 探讨电烧伤大鼠血管内皮生长因子(VEGF)和内皮素1(ET-1)的动态变化.方法 将大鼠64只随机分成2组:电烧伤组(56只)和对照组(8只).采用免疫组织化学方法测定伤后1d,3d,7d和14d的创周组织中VEGF的表达.采用ELISA方法测定烧伤后2h,6h,12h,24h血清ET-1的浓度.结果 伤后各个时间点创周组织VEGF蛋白表达均高于正常,VEGF表达在伤后第7天达到峰值.血清ET-1浓度显著升高,2h即明显高于正常值,6h达到峰值,此后逐渐下降,伤后24h仍明显高于正常.结论 电烧伤后VEGF和ET-1的表达均显著升高,这二种变化可能参与烧伤后微血管通透性的调节.     

肝硬化患者血浆ANP RIA及其临床意义

我们对60例肝硬化患者及40例正常人血浆心钠素(ANP)进行检测,结果表明,肝硬化患者血浆ANP水平显著高于正常人(P＜0.05),且与血清白蛋白浓度、凝血酶元时间和总胆固醇浓度分别相关.因此血浆ANP检测反映了肝脏受损程度及预后,有一定临床意义.     

Characterization of troponin responses in isoproterenol-induced cardiac injury in the Hanover Wistar rat

The investigations aimed to evaluate the usefulness of cardiac troponins as biomarkers of acute myocardial injury in the rat. Serum from female Hanover Wistar rats treated with a single intraperitoneal (IP) injection of isoproterenol (ISO) was assayed for cardiac troponin I (cTnI) (ACS: 180SE, Bayer), cTnI (Immulite 2000, Diagnostic Products Corporation) and cardiac troponin T (cTnT) (Elecsys 2010, Roche). In a time-course study (50.0 mg/kg ISO), serum cTnI (ACS:180SE) and cTnT increased above control levels at 1 hour postdosing, peaking at 2 hours (cTnI, 4.30 microg/L; cTnT, 1.79 microg/L), and declined to baseline by 48 hours, with histologic cardiac lesions first seen at 4 hours postdosing. The Immulite 2000 assay gave minimal cTnI signals, indicating poor immunoreactivity towards rat cTnI. In a dose-response study (0.25 to 20.0 mg/kg ISO), there was a trend for increasing cTnI (ACS:180SE) values with increasing ISO dose levels at 2 hours postdosing. By 24 hours, cTnI levels returned to baseline although chronic cardiac myodegeneration was present. We conclude that serum cTnI and cTnT levels are sensitive and specific biomarkers for detecting ISO induced myocardial injury in the rat. Serum troponin values reflect the development of histopathologic lesions; however peak troponin levels precede maximal lesion severity.     

Cardiac troponin I and cardiac troponin T increases in pigs during ischemia-reperfusion damage.

In this study we addressed the question of whether the measurement of cardiac Troponin T (cTnT) and cardiac Troponin I (cTnI) is able to detect myocardial cell damage in an ischemia-reperfusion model in pigs. To answer the question 3 pigs were anaesthesized and a cardiac arrest was induced by electric fibrillation. After 5 minutes of global ischemia the cardiac arrest was reversed by electric defibrillation until normal perfusion was restored. We could clearly demonstrate an increase of cTnT and cTnI 30 minutes after reperfusion indicating myocardial injury during ischemia and subsequent reperfusion. The cTnT as well as the cTnI serum levels increased till 180 minutes after reperfusion. This ischemia-reperfusion injury is likely induced by oxygen radicals generated during hypoxia and subsequent reperfusion We conclude from our first results that troponin measurements with commercial available test kits may also reflect myocardial cell damage in pigs as it was recently demonstrated in rats. Further studies are needed for correlation of troponin serum levels and histopathological damage in this model especially if it is used to test beneficial or toxicological effects of radical neutralizing drugs.     

Role of E-selectin for diagnosis of myocardial injury in children of age up to 14 years

Background: Effects of myocardial injury on E-selectin remain unclear. Thus, we investigated the diagnostic value of E-selectin for myocardial injury in children of no more than 14 years of age, which determined the scoring method of myocardial injury. Methods: In this prospective study, plasma E-selectin, cardiac troponin I (cTnI) and creatine kinase isoenzyme MB (CK-MB) concentrations in pediatric patients with myocardial injury (myocardial injury group, n=85) were measured. The control group comprised 80 patients without myocardial injury, and the case-control study method was selected at the same time. The definition of cardiac injury was based on cTnI and CK-MB (with or possibly without abnormal ECG evidence). Diagnostic value of E-selectin for myocardial injury was determined by analyzing receiver operating characteristic (ROC) curves. Results: The differences between the two groups were of statistical significance (P<0.001). For the 85 patients with myocardial injury, the area under the ROC curve (AUC) value for plasma E-selectin levels was 0.945 with a 95% CI of 0.899-0.991 and the optimal diagnostic cut-off value 29.67 ng/ml (positive likelihood ratio (positive LR=72.5); AUC value for plasma cTnI level was 0.848 with a 95% CI: 0.737-0.960 and the optimal diagnostic cut-off value was 0.155 µg/L (positive LR=12.3); AUC value for plasma CK-MB levels was 0.946 with a 95% CI: 0.903-0.989 and the optimal diagnostic cut-off value 24.26 IU/L (positive LR=72.5). Conclusions: E-selectin is more effective than cTnI in diagnosing myocardial injury as an important biological marker of myocardial injury- an important index of pediatric cardiac injury score.     

柚皮素对心肌缺血/再灌注损伤大鼠PI3K/AKT信号通路和内质网应激及其相关凋亡通路的影响

目的:观察柚皮素对缺血/再灌注(I/R)大鼠心脏损伤的影响,并探讨柚皮素的作用是否涉及PI3K/AKT信号通路和内质网应激及其相关凋亡通路.方法:48只SD大鼠按随机数字表法分成假手术组(sham组)、模型组(I/R组)、柚皮素处理组(NAR组)和柚皮素处理+LY294002组(NL组).结扎大鼠冠状动脉左前降支30 ...     

Troponin I: an update on clinical utility and method standardization

Cardiac troponin I (cTnI) is now widely recognized as one of the preeminent biochemical markers for the diagnosis of myocardial injury. The biochemical specificity of this biomolecule for cardiac tissue has forced a reevaluation of the diagnostic criteria for non-Q-wave acute myocardial infarction, unstable angina, acute coronary artery disease, and minor myocardial injury. Further, its use by clinicians has revolutionized the way that chronic and acute heart diseases are both diagnosed and managed. Unfortunately, the standardization of cardiac troponin I assays is problematic. Up to 20-fold variation of serum cTnI mass determinations may be observed for a given patient sample when measured by different assay systems. As a result, significant ambiguity often exists in the clinical interpretation of serum cTnI concentrations. Recent efforts have been directed toward the biochemical standardization of cTnI assays. However, the heterogeneous nature and biochemical complexity of the serum forms of cTnI and differences of the epitope recognition by the various methods have hindered the harmonization of serum cTnI assays.     

精胺上调大鼠心肌缺血再灌注时beclin-1的表达

目的:探讨精胺(SP)对大鼠心肌缺血再灌注(IR)无复流现象的影响及机制。方法:SD大鼠(220~250 g)随机分为IR组(缺血30 min/再灌注60 min)、IR+SP组(再灌注前15 min静脉注射0.5 mmol/L SP)和假手术对照组(实施开胸手术并穿线,但不结扎)。再灌注60 min后以Evans蓝和thilflavin S染色测定心肌无复流面积,HE染色观察心肌形态学改变,同时检测血浆中肌酸激酶同工酶MB(CK-MB)和心肌肌钙蛋白I(c Tn I)的含量及心肌组织中髓过氧化物酶(MPO)的活性。再灌注结束时,取左心室肌组织,Western blot法检测心肌组织中beclin-1的蛋白水平。结果:光镜下显示IR+SP组心肌的损伤与炎性浸润减轻;心肌无复流面积、血浆CK-MB和c Tn I的含量及心肌组织MPO的活性与IR组相比均减少(P0.05);Western blot结果显示IR+SP组的beclin-1表达较IR组增加(P0.05)。结论:外源性精胺能减轻大鼠心肌缺血再灌注损伤,其机制可能与上调beclin-1有关。     

Comparison of cardiac troponin I levels in serum and sodium-citrate plasma using the ACCESS 2 immunoassay

The aim of this study was to determine if sodium-citrate plasma is a suitable substitute for serum for cardiac troponin I (cTnI) measurement using the Beckman ACCESS 2 immunoassay. Linear regression analysis of cTnI levels in paired serum and sodium-citrate plasma samples from 80 patients provided a y-intercept of -0.0193 and a slope of 1.044. The correlation was good [r=0.995; 95% confidence interval 1.017 to 1.068, p <0.0001]. The paired results were not significantly different by Student's t-test. Serum and sodium-citrate plasma appear to be interchangeable as samples for cTnI measurement using the ACCESS 2 assay. Furthermore, the use of plasma reduces the turnaround time and may avoid false positive cTnI results due to residual fibrin.     

X线照射增加大鼠心肌对缺血/再灌注损伤的敏感性*

 目的：观察胸部X线放射治疗大鼠对心肌缺血/再灌注损伤的敏感性。方法：用胸部单次照射X线20 Gy构建放射性心脏损伤模型,采用完全随机分组方法将Wistar大鼠分为假损伤组、损伤组、假损伤+假手术组、假损伤+缺血/再灌注组、损伤+假手术组和损伤+缺血/再灌注组,于创伤后2周行心肌缺血/再灌注。通过BL-410生物信号记录分析系统记录各组大鼠左心室发展压（LVDP）、左心室压力上升的最大速率（+dp/dtmax）和左心室压力下降的最大速率（-dp/dtmax）;采用ELISA方法检测大鼠血清心肌肌钙蛋白I（cTnI）和肌酸激酶同工酶（CK-MB）;用BI2000图像分析软件测定心肌梗死面积占总面积的百分比。结果：损伤+缺血/再灌注组离体心功能明显低于假损伤+缺血/再灌注组（P＜0.01）,损伤+缺血/再灌注组血清cTnI和CK-MB水平显著高于假损伤+缺血/再灌注组（P＜0.01）,损伤+缺血/再灌注组心肌梗死面积显著大于假损伤+缺血/再灌注组（P＜0.01）。结论:X线照射增加大鼠心肌对缺血/再灌注损伤的敏感性。