心室肌致密化不全的研究进展

心室肌致密化不全(noncompaction of ventricular my-ocardium,NVM)是由于正常心室内膜在胚胎发育时受到抑制导致发育中的心肌小梁致密化失败,以持续存在无数粗大突起的肌小梁和小梁间深陷的隐窝[1]为特征的一种罕见的先天性心肌病,可孤立存在(isolated noncompaction ofthe ve     

心肌致密化不全的临床分析

心肌致密化不全(noncompaction of ventricular myocardium,NVM)是由于胚胎期心肌发育过程中心肌纤维及网状组织的致密化过程受阻所引起的一种心肌病,表现为无数突出于心室腔的肌小梁和深陷的小梁隐窝.临床表现有心衰、心律失常、栓塞等症状,无特异性,诊断困难,超声心动图对本病特征能够清晰显示,为诊断提供可靠依据.     

孤立性左室心肌致密化不全研究进展

左室心肌致密化不全(left ventricular noncompaction,LVNC)也称孤立性左室心肌致密化不全,是一种罕见的与遗传相关的未分类型心肌病,其病理特征表现为突出、粗大的左室肌小梁及与心腔相通的深小梁间隙、隐窝或窦状隙,且无证据表明其与心外膜冠状动脉系统相通,临床表现各异,常以进行性心功能不全、心律失常及血栓栓塞为主要表现。本文对LVNC 的病因、发病机制、临床表现、诊疗及预后进行综述,以指导LVNC 的临床诊疗.     

心肌致密化不全临床分析

心肌致密化不全(noncompaction of ventricular myocardium,NVM)是不定型心肌病的一种,为罕见的先天性心肌病,临床上常与扩张型心肌病相混淆[1].我院心内科因为心力衰竭就诊和住院的数千例患者中,确诊为NVM共10例,其临床表现和特征报告如下.     

值得重视的心肌病——心肌致密化不全

心肌致密化不全（noncompaction of ventricular mycardium，NVM）为一罕见的先天性疾病，有家族发病倾向，非单一遗传背景，可孤立存在（isolated noncompaction of ventricular mycardium，INVC），或与其他先天性心脏畸型并存。此病小儿多见，成人非常少见，但近年来关於成人发病的报导日见增多。国内有关报导较少，澳门未见有关报导，故将本院病例报导如下，并结合献报导予以综述。     

多普勒超声心动图对成人心肌致密化不全诊断价值的探讨

目的探讨超声心动图对心肌致密化不全（noncompaction of the ventricular myocardium,NVM）的诊断价值。方法采用超声心动图常规测量各腔室内径及心功能主要参数,分析二维、CDFI及频谱多普勒特点。结果①二维显示病变处心肌内外分为截然不同的两层,外层较薄,表现为回声较强的致密层,内层较厚,显示为为突出的肌小梁及深陷其问的隐窝,呈＂蜂窝状＂,好发于左心室心尖部、侧壁。左房室增大,可合并室壁隐窝或房室腔内血栓形成。②病变处心内膜呈波浪状。③M型超声心动图显示该处室壁运动幅度低平,收缩期室壁增厚率下降。④多普勒超声心动图显示深陷于肌小梁间的隐窝内可见血流信息,并与心室腔相通。结论NVM具有特征性超声改变,彩色多普勒超声心动图是无创、敏感诊断心肌致密化不全的首选方法。     

超声心动图对心肌致密化不全的诊断价值

目的探讨超声心动图对心肌致密化不全（noncompaction of the ventricular myocardium,NVM）的诊断价值及临床意义。方法彩色多普勒超声心动图对临床心功能不全及心脏扩大的患者进行多切面的探查,以获取心脏形态、结构及血流信号。结果 28例超声诊断为NVM,其中26例为左心室受累,2例右心室受累,采用詹尼（Jenni）等提出的诊断标准,其内容包括：（1）不合并其他心脏畸形（孤立性心肌致密化不全）;（2）左室部分室壁增厚分为两层,致密层较薄而非致密层较厚;（3）收缩末期非致密化层/致密化层比例〉2;（4）UCG可见心室与小梁隐窝间有血流交通。病变部位：位于心尖部,合并下壁6例,合并侧壁5例,心室壁均未见血栓形成。结论 NVM具有特征性声像图表现,是诊断NVM的可靠首选的检查手段。     

彩色多普勒超声心动图对心肌致密化不全诊断价值的探讨

目的 探讨超声心动图对心肌致密化不全(noncompaction of the ventricular myocardium,NVM)的诊断价值及临床意义,以提高临床及超声医师对该病的认识.方法 用二维、M型及多普勒超声心动图对疑似病人进行多方位、多切面的探查,以获取其心脏形态、结构及血流信息改变特征,进行观察分析.结果 ①二维显示病变处心肌内外分为截然不同的两层,外层较薄,表现为回声较强的致密层,内层较厚,显示为为突出的肌小梁及深陷其间的隐窝,呈"蜂窝状",好发于左心室心尖部、侧壁.左房室增大,可合并室壁隐窝或房室腔内血栓形成.②病变处心内膜呈波浪状.③M型超声心动图显示该处室壁运动幅度低平,收缩期室壁增厚率下降.④多普勒超声心动图显示深陷于肌小梁间的隐窝内可见血流信息,并与心室腔相通.⑤晚期患者受累心功能减低.结论 NVM具有特征性声像图表现,超声心动图在无明显症状阶段即可诊断,是诊断NVM的较可靠而简便的检查手段.     

心肌致密化不全彩色多普勒超声诊断价值

心肌致密化不全（noncompacdon of the ventficular myocardium．NVM）是一种少见的先天性心肌病．又称海绵样心肌或心肌窦状持续状态．是胚胎发育早期．网络状肌小梁致密化过程失败导致小梁化的心肌持续存在．以无数突出的肌小梁和深陷隐窝为特征。可孤立存在或与其他先天性心脏畸形并存,临床上易与扩张型心肌病及缺血性心肌病等相混淆．     

超声心动图诊断心肌致密化不全

心肌致密化不全（NVM）,过去称为＂海绵样心肌＂或＂心肌窦状隙未闭＂是一种少见的先天性心脏病,直至1990年美国的Chin等[1]将其正式命名为＂NVM＂。NVM是以胚胎发育5～6周网织结构的肌小梁,小梁间深陷的隐窝和心室收缩功能减退为其特征。     

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.     

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.     

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     

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.