应用斑点追踪显像技术评价肥厚心肌应变的效果观察

目的 探讨二维斑点追踪显像(2DSTI)技术评价肥厚心肌的左心室功能的价值.方法 选择正常对照组30例,高血压心肌肥厚组30例,糖尿病心肌肥厚组30例.应用STI技术测定左心室各壁基底段、中间段和心尖段收缩期峰值应变(Ls),并对检测结果进行分析.结果 与对照组相比,高血压心肌肥厚组与糖尿病心肌肥厚组的心肌纵向应变值在左室基底段和中间段、心尖段均较对照组低(P＜0.05).与糖尿病心肌肥厚组比较,高血压合并心肌肥厚组在左室基底段、中间段和心尖段的纵向应变值差异无统计学意义(P＞0.05).结论 应用二维斑点追踪显像技术测量收缩期左室径向应变值,可以了解心肌收缩时径向运动和应变值的变化,有助于判断和评价局部心肌功能.     

完全性左束支传导阻滞患者左心室心肌收缩功能的研究

目的 应用超声二维斑点追踪显像技术探讨完全性左束支传导阻滞患者左室心内膜下心肌收缩功能.方法 完全性左束支传导阻滞患者(CLBBB)20例,正常对照者20例,采用心尖长轴四腔心和二腔观的二维灰阶动态图像,应用二维应变软件测量左室壁各节段的心内膜下心肌收缩应变、应变率及整体长轴应变(GLS),心尖双平面Simpson法测量左室射血分数(LVEF﹑FS%).结果 与正常组比较,LBBB组,的左房内径、E/A、左室长轴心内膜下心肌的纵向收缩期峰值应变、应变率减低(P<0.05).结论 超声二维斑点追踪显像技术能准确地评价左束支患者的左室心内膜下心肌收缩功能.     

二维斑点技术评价糖尿病患者的心肌收缩功能和同步性

目的 探讨二维斑点技术评价糖尿病患者的心肌收缩功能和同步性。方法 从本院收治的糖尿病患者选择40例,并选取同期38名健康者为本次的研究对象,所有人使用二维斑点超声技术,获取心尖四腔观、两腔观、左室长轴观图像,各水平段的左室短轴观图像,并对内膜下及外膜下心肌收缩期的纵向、圆周向、径向峰值应变,左心室收缩同步性进行测定。结果 两组的LVEDD、LVESD、LVFS、IVSd、PWd、LVEF、二尖瓣E峰值、二尖瓣A峰值、E/A等常规超声心动图指标均有差异,但差异无统计学意义（P> 0.05）。左室长轴内膜下心肌收缩期纵向峰值应变中,研究组与对照组相比显著更低（P <0.05）;外膜下心肌收缩期纵向峰值应变中,后壁、下壁及后间隔显著更低（P <0.05）。研究组的基底段内外膜下、中间段内外膜下、心尖段内外膜下左室短轴心肌收缩期圆周向峰值应变较对照组显著更低（P <0.05）,尤其是基底段、中间段内膜下降低更明显（P <0.05）。两组的左室短轴心肌收缩期径向峰值应变均差异无统计学意义（P> 0.05）。对照组的心底水平旋转曲线波形为负向,心尖水平为正向,曲...     

二维超声斑点追踪技术评价肾功能不全患者左室整体收缩功能

目的：应用二维超声斑点追踪技术（2D-STI）评价肾功不全患者左心室收缩功能。方法：正常对照组20例，肾功不全患者32例，常规二维超声测量左室舒张末期容积、左室收缩末期容积获取左室射血分数。取乳头肌水平左室短轴连续3个心动周期的二维动态图像，分析计算各节段的左室短轴应变参数，将上述指标进行两组间对比分析。结果：与正常对照组比，RF组EDV、ESV显著增大，EF减低（P＜0.05）。RF组室壁各节段收缩期峰值径向应变均低于正常对照组（P〈0.05）。结论2D-STI作为一种新技术能客观、定量评价肾功不全患者左心室收缩功能。     

二维斑点追踪成像技术对糖尿病心肌病患者左室收缩功能的诊断

目的应用斑点追踪成像技术研究正常人及糖尿病心肌病患者的左心室长轴纵向、短轴径向及圆周应变改变规律,探讨其临床应用价值。方法获取正常对照组(21例)、糖尿病心肌病组(17例)标准心尖四腔、三腔、两腔和短轴二尖瓣、乳头肌、心尖水平图像;分别测量和比较糖尿病心肌病组与正常对照组各节段的纵向、径向和圆周的收缩期峰值应变。结果正常组左室长轴纵向应变在心尖部最大(P<0.05);短轴径向应变差异无统计学意义;圆周应变在室间隔及前间隔较其他室壁节段高(P<0.05)。与对照组比较,糖尿病心肌病组,纵向、短轴径向及圆周应变平均值均降低(P<0.05)。结论斑点成像技术能够较好的评价糖尿病心肌病左室整体和局部的收缩功能。     

超声三维斑点追踪成像技术评价2型糖尿病患者左室整体收缩功能与左室重构的相关性

目的应用超声三维斑点追踪成像技术（3-dimensional Speckle Tracking Imaging,3D-STI）评价2型糖尿病（T2DM）患者左室整体收缩功能与左室重构的关系。方法选取60例T2DM患者（正常构型组30例、左室重构组30例）和30例健康志愿者,应用3D-STI测量并比较各组左室舒张末容积（LVEDV）、左室收缩末容积（LVESV）、左室质量指数（LVMI）、左室射血分数（LVEF）、左室整体纵向收缩期峰值应变（LVGLS）、左室整体径向收缩期峰值应变（LVGCS）、左室整体环向收缩期峰值应变（LVGRS）。结果与正常对照组相比,A组LVMI、LVEDV、LVESV均增大且差异有统计学意义（P〈0.05）,LVGLS、LVGCS、LVGRS均减小且差异有统计学意义（P〈0.05）,LVEF差异无统计学意义（P＆gt;0.05）;B组较A组LVEDV、LVESV、LVMI增大且差异有统计学意义（P〈0.05）,LVEF、LVGLS、LVGCS、LVGRS均减小且差异有统计学意义（P〈0.05）。T2DM组LVMI与LVGLS、LVGCS、LVGRS、LVEF呈显著负相关（r=-0.63,-0.65,-0.69,-0.78,均P〈0.05）。结论 T2DM患者可出现不同程度的左室重构,且随着重构的发展,左室整体收缩功能降低。3D-STI可无创、客观地评价左室整体收缩功能,具有重要的临床指导意义。     

左室整体心肌及心内膜下心肌短轴应变在糖尿病早期心功能诊断中的价值

目的应用斑点追踪成像技术评价糖尿病患者及糖尿病合并高血压患者左室短轴心内膜下心肌早期的收缩功能。方法 3组检测对象分别为单纯糖尿病组、糖尿病合并高血压组及对照组各30例。应用超声心动图测量常规参数及应用超声斑点追踪成像技术测量左室短轴整体及心内膜下心肌不同水平各节段二维应变值,比较3组间的差异。结果 3组间的常规参数比较,糖尿病组E/A比值的变化差异有统计学意义(P<0.01)。3组间的不同水平节段二维应变值比较,糖尿病组及糖尿病合并高血压组左室短轴整体心肌部分节段二维应变有所减低(P<0.01);糖尿病组及糖尿病合并高血压组左室短轴心内膜下心肌大部分节段二维应变均减低(P<0.01),其中糖尿病合并高血压组心内膜下心肌部分节段比单纯糖尿病组更低(P<0.01)。结论斑点追踪成像技术能早期发现局部心肌功能的改变,可以作为监测糖尿病心肌损伤的一个重要参考指标。     

超声斑点追踪成像技术评价短期药物干预对高血压大鼠左心功能的影响

目的 应用超声斑点追踪成像技术(STI)观察短期药物干预对自发性高血压大鼠(SHR)左室节段心肌径向(RS)及圆周应变(CS)的变化,探寻较传统超声心动图更早评价左室收缩功能改变的方法 . 方法 以10只Wistar大鼠为正常对照组,将30只SHR随机分成对照组、硝苯地平组、三子养阴汤组各10只,分别测量左室EF,FS及左室短轴乳头肌水平RS和CS的收缩期峰值. 结果4组大鼠的EF、FS值无明显差异,模型对照组大鼠的PRS和PCS明显降低(P<0.05),与模型对照组比较,硝苯地平组PRS除了下壁与间隔外,其余4个节段明显升高(P<0.05),三子养阴汤组6个节段PCS降低,以前间隔、前壁、侧壁、后壁为著(P<0.05). 结论 STI能定量评价左室局部心肌的RS和CS,较传统超声更为敏感.     

应用三维斑点追踪技术评价肥厚型心肌病患者左室功能的价值

目的应用实时三维斑点追踪定量技术评估肥厚型心肌病患者左室整体应变功能。方法选取36例肥厚型心肌病患者和25例正常对照组,通过三维斑点追踪技术测量左室心肌整体纵向、径向、圆周、及面积峰值应变值,进行比较分析。结果与对照组比较,肥厚型心肌病组左室心肌整体纵向应变、径向应变、面积应变、圆周应变等指标均减低,差异有统计学意义(P<0.05);GLS、GAS与左室舒张末期室间隔的最大厚度相关性良好(r=0.82、0.78,P<0.05);HCM组与对照组的LVEDV、LVESV、LVEF的传统心脏功能指标比较,差异无统计学意义(P>0.05)。结论 RT3D-STI评价肥厚型心肌病左室心肌功能准确、可行,为临床早期诊断提供了有价值的信息。     

斑点追踪技术评价缺血心肌的运动速度

目的探讨斑点追踪技术(STI)评价缺血心肌运动速度的应用价值。方法对30例心肌缺血患者和26例正常对照组行超声心动图检查,分别记录左室短轴观(二尖瓣水平)的高帧频二维灰阶图像,应用Qlab定量分析软件测量各节段心肌的收缩期峰值速度(speed)和径向峰值速度(radial-velocity)。结果心肌缺血组收缩期峰值速度和径向峰值速度均明显低于正常对照组,差异有统计学意义(P0.05)。结论斑点追踪技术能对缺血心肌的运动速度进行定量分析,评价局部心肌功能。     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.     

Hyperkalaemia in patients in hospital

A survey of all laboratory blood specimens with a plasma potassium concentration greater than or equal to 5.5 mmol/L was conducted over a three month period. Of 331 specimens with hyperkalaemia, 71 were excluded because the specimens was haemolysed, old or contaminated. The laboratory served a population of 348,561 and during this time measured the plasma potassium on 25,016 occasions. Sixty-six outpatients and 20 neonates were not evaluated. The survey was undertaken on 86 of 102 inpatients (46 males), 48 of whom were over 66 years of age. Fifty-seven patients were admitted under a medical service and 29 under a surgical service. Fifty-nine had a single episode of hyperkalaemia. Thirty-two underwent a surgical procedure. The commonest contributing factor was impaired renal function which was present in 71 (83%) patients. Although a definitive causative role for drugs could be identified in only five patients, in 52 (60%) patients drugs were a contributing factor (potassium supplements 24, ACE inhibitors 16, nonsteroidal antiinflammatory drugs 12). Thirty-five of the 86 (41%) patients died during their hospital admission. Nineteen of the 35 deaths occurred within three days of the hyperkalaemia being recorded. A normal plasma potassium was eventually documented in 50 of the 86 patients. Of the remaining 36 patients, 25 (69%) subsequently died. In general the treatment of patients with hyperkalaemia focused on identifying and treating the underlying cause. Hyperkalaemia must always be considered seriously and regard given to the overall clinical status of the patient, with particular attention to drug therapy, renal and cardiac function, acid base status and the possibility of sepsis.