大鼠胸主动脉缩窄诱导心肌肥厚模型的建立

目的建立大鼠胸主动脉部分缩窄诱导心肌肥厚动物模型。方法雄性SD大鼠30只,随机分为两组：胸主动脉缩窄组20只和同期假手术组10只。在右无名动脉和左颈总动脉之间将主动脉结扎于8G针头上,随后将针头退出即可。术后10周,采用超声心动图检测心脏、观察心脏的大体剖面以及HE染色、测量心肌肥厚指数评价心肌肥厚的效果。结果术后10周,肉眼观：模型组心脏体积明显大于对照组。M型超声示：模型组较假手术组缩短分数下降,左室内径和室壁厚度明显增加。超声测量结果示：模型组与假手术组比较：室间隔厚度增加明显（2.527±0.269 vs.1.943±0.1）mm,（P〈0.01）;后壁厚度增加明显（2.492±0.242 vs.1.902±0.076）mm,（P〈0.01）;缩短分数略减小（49±7.681 vs.55.7±9.828）（P〉0.05）;左室舒张末期内径、左室收缩末期内径及射血分数均无明显变化。心脏肥厚指数明显增大（3.196±0.11 vs.1.785±0.099）,P〈0.01。结论胸主动脉缩窄可以导致大鼠心肌肥厚,为研究心室肥厚、心肌功能障碍以及心肌重构提供了一个很好的模型。     

15例儿童心动过速性心肌病的诊疗体会

目的:探讨儿童完全性心动过速性心肌病(pTIC)的临床特点、治疗及预后。方法:回顾分析2009年1月至2016年10月安徽省儿童医院心内科收治的15例完全性心动过速性心肌病患儿的临床表现、心功能、心电图、心脏彩超的特点,观察心律失常控制后的心室率、心脏左室内径大小及心功能恢复情况。结果:15例pTIC患儿以室上性快速心律失常多见(14例),10例单纯药物治疗,3例接受射频消融转为窦性心律,2例失访。随访半年至3年与治疗前比较心室率明显下降[(116±27)次/分vs.(189±28)次/分]、NT-proBNP降低[(404±355)pg/mL vs.(6280±3155)pg/mL]、心脏左室舒张末内径变小[(3.12±0.48)cm vs.(3.69±0.70)cm]、左室射血分数升高[(57.9±9.3)%vs.(42.2±9.5)%]、改良ROSS评分下降[1(0-5)分vs.7(4-10)分]。结论:儿童pTIC由各种快速心律失常引起,心脏扩大和心功能障碍可完全恢复,早期识别、有效治疗的儿童pTIC长期预后良好。     

超声心动图对心肌致密化不全的诊断及临床意义探讨

目的:探讨超声心动图对心肌致密化不全的诊断及临床意义。方法:应用Vivid7、HP5500彩色多普勒超声诊断仪(探头频率为2～4MHz)对32例左室心肌致密化不全患者进行检查,采用二维、M型、彩色及频谱多普勒观察病变心肌及心内膜改变,重点观察心尖段。常规测量各腔室内径、左室壁正常段心肌厚度及动度,评价心室舒张功能、计算左心室射血分数EF及瓣膜反流等基本信息。结果:①受累的心室内膜面可见多发异常粗大的、呈蜂窝状的肌小梁和交错深陷的隐窝形成网状结构。②病变区域心室壁外层的致密心肌明显变薄,为中低回声,较正常心肌薄2~4mm,其心肌厚度<6mm,而内层心肌疏松增厚为强回声。③病变以近心尖部1/3室壁节段最为明显,很少累及室间隔及基底段室壁。④彩色多普勒可示隐窝间隙之间有低速血流与心腔相通。⑤多数患者以渐进性的心功能不全、呼吸困难、体循环栓塞、心律失常为主要表现,本组患者临床表现为心力衰竭22例,心脏杂音3例,心律失常2例,5例无明显不适症状。结论:超声心动图检查是准确、无创诊断心肌致密化不全的首选方法,能够对房室结构和心功能进行全面评价,有助于明确心力衰竭病因并协助治疗,同时也有助于筛查心肌致密化不全家族,对临床治疗起着很好的指导作用。     

生脉注射液联合曲美他嗪治疗缺血性心肌病合并肾功能不全的临床疗效分析

目的:研究生脉注射液联合曲美他嗪治疗缺血性心肌病合并肾功能不全的临床疗效。方法:选取2015年3月至2017年3月我院收治的100例缺血性心肌病合并肾功能不全患者,按照随机数表法分为观察组(n=50)和对照组(n=50)。对照组采用曲美他嗪治疗,观察组采用生脉注射液联合曲美他嗪治疗。观察和比较两组的治疗疗效、治疗前后心功能指标(左心室射血分数(LVEF)、左室收缩末径(LVESD)、左室舒张末期内径(LVEDD))、肾功能指标(血肌酐(Scr),尿素氮(BUN))、心肌损伤标志物(血清胱抑素(Cys C)、同型半胱氨酸(HCY)、脑钠肽(BNP))水平的变化。结果:治疗后,观察组总有效率显著高于对照组[92.30%(48/52) vs.70.83%(34/48)](P0.05),LVEDD、LVESD水平均显著低于对照组[(51.21±8.54)mm vs.(56.63±10.83)mm,(42.91±6.30)mm vs.(45.86±7.32)mm](P0.05),LVEF水平均显著高于对照组[(46.02±7.85)%vs.(41.20±8.84)%](P0.05),Scr、BUN水平均显著低于对照组[(164.30±17.95)μmol/L vs.(211.75±19.31)μmol/L;(8.12±0.76)mmol/L vs.(11.74±1.72)mmol/L](P0.05)。血清Cys C、HCY、NT-Pro BNP水平均显著低于对照组[(0.90±0.21)mg/L vs 1.52±0.34)mg/L (12.34±3.89)μmol/L vs.(20.86±5.28)μmol/L,(298.47±78.41)ng/L vs.(402.35±92.76)ng/L](P0.05)。结论:生脉注射液联合曲美他嗪治疗缺血性心肌病合并肾功能不全的的临床疗效显著优于单用曲美他嗪治疗,其可有效改善患者心、肾功能,减轻心肌细胞损伤。     

超声心动图对心肌致密化不全的诊断及临床意义探讨

目的：探讨超声心动图对心肌致密化不全的诊断及临床意义。方法：应用Vivid7、HP5500彩色多普勒超声诊断仪（探头频率为2～4MHz）对32例左室心肌致密化不全患者进行检查,采用二维、M型、彩色及频谱多普勒观察病变心肌及心内膜改变,重点观察心尖段。常规测量各腔室内径、左室壁正常段心肌厚度及动度,评价心室舒张功能、计算左心室射血分数EF及瓣膜反流等基本信息。结果：①受累的心室内膜面可见多发异常粗大的、呈蜂窝状的肌小梁和交错深陷的隐窝形成网状结构。②病变区域心室壁外层的致密心肌明显变薄,为中低回声,较正常心肌薄2~4mm,其心肌厚度〈6mm,而内层心肌疏松增厚为强回声。③病变以近心尖部1/3室壁节段最为明显,很少累及室间隔及基底段室壁。④彩色多普勒可示隐窝间隙之间有低速血流与心腔相通。⑤多数患者以渐进性的心功能不全、呼吸困难、体循环栓塞、心律失常为主要表现,本组患者临床表现为心力衰竭22例,心脏杂音3例,心律失常2例,5例无明显不适症状。结论：超声心动图检查是准确、无创诊断心肌致密化不全的首选方法,能够对房室结构和心功能进行全面评价,有助于明确心力衰竭病因并协助治疗,同时也有助于筛查心肌致密化不全家族,对临床治疗起着很好的指导作用。     

地高辛联合左西孟旦治疗扩张型心肌病的疗效及对血清HMGB1、sICAM-1、sST2水平的影响

目的:探讨地高辛联合左西孟旦治疗扩张型心肌病的疗效及对血清高迁移率族蛋白B1(HMGB1)、溶性细胞间粘附分子-1(s ICAM-1)、可溶性ST2蛋白(s ST2)水平的影响。方法：选择2016年2月至2018年2月我院接诊的90例扩张型心肌病患者作为本研究对象,依照随机数表法分为观察组44例和对照组46例,对照组在常规治疗基础上给予左西孟旦治疗,观察组在对照组基础上联合地高辛治疗,两组均连续治疗4周。比较两组的临床疗效、左室射血分数(LVEF)、左室舒张末内径(LVEDD)、血清氨基末端B型钠尿肽前体(NT-proBNP)、HMGB1、s ICAM-1、s ST2水平的变化及不良反应的发生情况。结果:治疗后,观察组临床疗效总有效率为93.18%(41/44),明显高于对照组(76.09%,P0.05);观察组LVEF明显高于对照组,LVEDD、血清NT-proBNP水平均明显低于对照组[(46.50±5.21)%vs.(41.20±4.12)%,(54.94±2.29)mm vs.(59.30±2.38)mm,(494.31±75.95)ng/L vs.(589.56±89.40)ng/L](P0.05);观察组血清HMGB1、s ICAM-1、s ST2水平均明显低于对照组低[(8.42±1.23)pg/mL vs.(13.76±1.70)pg/mL,(122.93±11.03)μg/L vs.(141.58±13.04)μg/L,(0.08±0.02)ng/mL vs.(0.15±0.03)ng/mL](P0.05)。治疗期间,两组不良反应发生率分别为9.09%和6.52%,组间差异无统计学意义(P0.05)。结论:地高辛联合左西孟旦治疗扩张型心肌病患者的效果显著优于单用左西孟旦治疗,其可更有效降低患者血清HMGB1、s ICAM-1、s ST2的表达,改善患者心功能,且安全性高。     

缺血性心肌病的多模态心血管影像学方法进展

近年来,超声(ultrasound, US)、CT冠状动脉造影(CT coronary angiography, CCTA)、血管内超声(intravenous ultrasound,IVUS)、光学相干断层成像(optical coherence tomography, OCT)、多层螺旋CT成像(multi-slice computed tomography, MSCT)、单光子发射计算机断层成像(single-photon emission computed tomography, SPECT)、正电子发射计算机断层成像(positron emission computed tomography, PET)及心脏磁共振(cardiac magnetic resonance, CMR)等多种心血管成像技术能够提供与冠脉病变及心肌形态和功能相关的解剖学、血流动力学、细胞生物学及病理生理学等方面的重要信息,在缺血性心肌病的临床诊疗及预后评估中发挥着日益重要的作用。然而,如何恰当选择的多模态心血管影像技术是临床医师面临的一大难题。因此,本文在归纳总结主要心血管成像技术临床应用进展的基础上,对多模态心血管影像学在缺血性心肌病相关的冠脉解剖与斑块成像、心肌功能、心肌灌注及心肌活性显像中的临床应用价值进行综述。旨在帮助临床医师客观认识各种成像技术的优势与不足,从而制定最优化的选择方案。     

血清Irisin水平与心衰的相关性研究

目的:观察心衰患者血清IRISIN水平变化规律,研究Irisin对心衰诊疗的临床价值。方法:连续收集西京医院心内科住院的心衰患者132例,根据NYHA心功能分级将患者分为三组,其中心功能Ⅱ级48例,Ⅲ级44例,Ⅳ级40例,同时选取心功能正常(左室射血分数LVEF50%)的30例健康体检者为对照组。采用酶联免疫吸附试验(ELISA)检测患者血清中Irisin水平,根据Irisin水平分为低Irisin组和高Irisin组,比较两组间心衰的发生率,分析Irisin水平与心衰的关系。结果:①心衰组Irisin水平显著低于心功能正常组(6790±3628 ng/mL vs 12691±2272 ng/mL,P0.01),且从Ⅱ级到Ⅳ级,逐渐降低;②心衰组LVEF值显著低于心功能正常组(45.7±8 vs 59.7±4.3,P0.01),且从Ⅱ级到Ⅳ级,逐渐降低;③心衰组N末端B型利钠肽原(ProBNP)水平显著高于心功能正常组(2938±2795 pg/mL vs 184±151 pg/mL,P0.01),且从Ⅱ级到Ⅳ级,逐渐升高;④低Irisin组心衰发生率明显高于高Irisin组(92.6%vs47.5%,P0.01);⑤单因素相关分析显示:血清Irisin水平与左室射血分数呈正相关(r=0.694,P0.05),与proBNP呈负相关(r=-0.45,P0.05);结论:心衰患者血清Irisin水平降低,而且随着心功能的恶化显著降低,心衰患者血清Irisin水平与心衰程度有一定的相关性。     

探讨超声心动图对心肌致密化不全的诊断及指导治疗价值

目的研究心肌致密化不全的心内结构及心功能的改变,探讨超声心动图对心肌致密化不全的诊断及指导治疗的价值。方法常规检查各切面,主要测量房室内径、室壁厚度及运动幅度、瓣膜血流情况、心功能指数,重点了解室壁心肌结构及舒张末期左室内径、左心室射血分数,观察房室腔内是否有血栓形成。结果 3例患者中有2例单独左心室受累,1例累及双心室。3例患者超声心动图上均有特征性改变,心室内均见异常隆突的肌小梁和深陷其间的隐窝,彩色多普勒超声见肌小梁隐窝内的血流信号与心室腔相通。病变好发于左室心尖部、侧壁、下后壁,伴或不伴心功能不全、心律失常。结论对心肌致密化不全超声心动图具有特征性声像图表现,其检查能够对心肌致密化不全进行房室结构及功能的全面评价,是发现心肌致密化不全的首要方法,也是定期观察治疗后心功能改善的必要手段。     

缺血性心肌病大鼠心肌细胞自噬在心肌重塑中的作用*

目的:研究缺血性心肌病大鼠心肌细胞自噬在心肌重塑中的作用。方法:36 只雄性SD大鼠分为正常对照组、假手术组、缺血性心肌病组( n=12),3组大鼠术前行心脏彩超检查,正常对照组大鼠不进行处理;假手术组大鼠开胸后不结扎冠状动脉,关闭胸腔;缺血性心肌病组大鼠开胸结扎冠状动脉20 min后,解开结扎线行再灌注后关闭胸腔,3组大鼠术后4周行心脏彩超检查后处死大鼠取心脏行HE染色、masson染色,观察心肌病理改变,用Western blot技术检测各组大鼠心肌细胞GRP78、LC3-I、LC3-II、Beclin-I表达及LC3-II/LC3-I比值的变化。结果:与正常组及假手术组比较,缺血性心肌病大鼠心室扩大,EF值降低;心肌排列紊乱,心肌纤维化增加;线粒体空泡化严重;内质网应激关键蛋白GRP78上调;自噬相关蛋白LC3-I、LC3-II、Beclin-I及LC3-II/LC3-I比值增加。结论:缺血性心肌病大鼠心肌细胞中内质网应激和自噬可能在心肌重塑中具有重要作用。     

Cadaveric cardiosphere-derived cells can maintain regenerative capacity and improve the heart function of cardiomyopathy

Objective: Cardiosphere-derived cells (CDCs) improve cardiac function and attenuate remodeling in ischemic and non-ischemic cardiomyopathy, and are currently obtained through myocardial biopsy. However, there is not any study on whether functional CDCs may be obtained through cadaveric autopsy with similar benefits in non-ischemic cardiomyopathy. Methods: Cardiac tissues from human or mouse cadavers were harvested, plated at 4°C, and removed at varying time points to culture human CDCs (CLH-EDCs) and mouse CDCs (CM-CDCs). The differentiation and paracrine effects of CDCs were also assessed. Furthermore, intramyocardial injection of cadaveric CM-CDCs was performed in an induced dilated cardiomyopathy (DCM) model. Results: With the extension of post mortem hours, the number of CLH-EDCs and CM-CDCs harvested from autopsy specimens decreased. The expressions of von Willebrand factor (VWF) and smooth muscle actin (SMA) on CDCs were gradually reduced, however, cardiac troponin I (TNI) expression increased in the 24 h group compared to the 0 h group. CLH-EDCs were also found to have similar paracrine function in the 24 h group compared to 0 h group. 8 weeks after CM-CDCs transplantion to the injured heart, mean left ventricular ejection fraction increased in both 0 h (64.99 ± 3.4%) and 24 h (62.99 ± 2.8%) CM-CDCs-treated groups as compared to the PBS treated group (53.64 ± 5.6 cm), with a decrease in left ventricular internal diastolic diameter (0.29 ± 0.08 cm and 0.32 ± 0.04 cm in 0 h and 24 h groups, vs. 0.41 ± 0.05 cm in PBS group). Conclusion: CDCs from cadaveric autopsy are highly proliferative and differentiative, and may be used as a source for allograft transplantation, in order to decrease myocardial fibrosis, attenuate left ventricular remodeling, and improve heart function in doxorubicin-induced non-ischemic cardiomyopathy.     

Stimulatory guanine nucleotide-binding protein and adenylate cyclase activities in Bio 14.6 cardiomyopathic hamsters at the hypertrophic stage

The Bio 14.6 cardiomyopathic Syrian hamster is an animal model of human idiopathic cardiomyopathy. The pathogenesis of the disease in this animal has not yet been clearly elucidated. It is well known that α- and β-adrenergic receptors are increased in the myocardium of this animal, but that isoprenaline does not produce an augmented response. We examined the activity of cardiac stimulatory GTP-binding protein (Gs), which couple with β-adrenergic receptors to stimulate adenylate cyclase, in Bio 14.6 cardiomyopathic hamsters at 90 and 160 days of age. The cardiac norepinephrine concentration was significantly increased in Bio 14.6 hamsters compared with control hamsters (F1B) at 90 days of age (1,739±120 vs 1,470±161 ng/g wet tissue weight, p<0.05). Cardiac forskolin-stimulated adenylate cyclase activities at 90 and 160 days of age were lower in the cardiomyopathic hamsters than in the F1B controls (90 days old: 98±24 vs 122±29 pmol/min/mg protein, p<0.05; 160 days old: 74±13 vs 124±28 pmol/min/mg protein, p<0.01). Cardiac Gs activities at 90 and 160 days of age were significantly lower in Bio 14.6 hamsters than those in F1B hamsters (90 days old: 204±42 vs 259±49 pmol/min/mg protein, p<0.05; 160 days old: 156±39 vs 211±60 pmol/min/mg protein, p<0.05). We thus demonstrated functional defects in cardiac Gs protein and adenylate cyclase activity in the Bio 14.6 cardiomyopathic hamsters at 90 to 160 days of age (the hypertrophic stage of cardiomyopathy). Such defects could be one possible mechanism preventing an enhanced response to β-adrenergic stimulation in this animal and could also contribute to myocardial decompensation in the late stage of cardiomyopathy.     

缺血性脑卒中患者血清超敏C反应蛋白、糖化血红蛋白水平及其与神经功能缺损的关系

目的:探讨缺血性脑卒中患者血清超敏C反应蛋白(hs-CRP)、糖化血红蛋白(HbA1c)水平及其与神经功能缺损的关系。方法:选择2016年10月~2017年9月我院接诊的123例缺血性脑卒中患者作为观察组及同期于我院进行体检的健康人群123例作为对照组,检测和比较两组血清hs-CRP、HbA1c水平的差异,并分析缺血性脑卒中患者血清hs-CRP、HbA1c水平与其美国国立卫生研究院卒中量表(NIHSS)评分的关系。结果:观察组患者血清hs-CRP、Hb A1c水平显著高于对照组[(6.23±1.97)mg/L、(7.96±0.65)%vs.(2.54±0.85)mg/L、(5.21±0.30)%],NIHSS评分明显高于对照组[(4.08±3.12)分vs. 8.62±3.25)分],差异具有统计学意义(P0.05);缺血性脑卒中患者血清hs-CRP、Hb A1c水平与NIHSS评分呈显著正相关(r=-0.465,-0.564,P0.05)。结论:缺血性脑卒中患者血清hs-CRP和HbA1c水平均明显上调,二者可以在一定程度上反映缺血性脑卒中患者神经功能缺损的严重程度。     

Three-dimensional speckle tracking echocardiography and cardiac magnetic resonance for left ventricular chamber quantification and identification of myocardial transmural scar

Background

We compared three-dimensional speckle tracking echocardiography (3DSTE) and its strain to cardiac magnetic resonance (CMR) with delayed contrast enhancement for left ventricular (LV) chamber quantification and transmurality of myocardial scar. Furthermore, we examined the ability of 3DSTE strain to differentiate between ischaemic and non-ischaemic LV dysfunction.

Methods

In 80 consecutive patients with ischaemic and 40 patients with non-ischaemic LV dysfunction, the correlations between LV volumes and ejection fraction were measured using 3DSTE and CMR. Global and regional 3DSTE strains and total or percentage enhanced LV mass were evaluated.

Results

LV end-diastolic and end-systolic volumes and ejection fraction correlated well between 3DSTE and CMR (r: 0.83, 0.88 and 0.89, respectively). However, 3DSTE significantly underestimated volumes. Correlation for LV mass was modest (r = 0.59). All 3DSTE regional strain values except for radial strain were lower in segments with versus segments without transmural enhancement. However, strain parameters could not identify the transmurality of scar. No significant difference between ischaemic and non-ischaemic LV dysfunction was observed in either global or regional 3DSTE strain except for twist, which was lower in the non-ischaemic group (4.9 ± 3.3 vs. 6.4 ± 3.2°, p = 0.03).

Conclusion

3DSTE LV volumes are underestimated compared with CMR, while LV ejection fraction revealed excellent accuracy. Functional impairment by 3DSTE strain does not correlate well with scar localisation or extent by CMR. 3DSTE strain could not differentiate between ischaemic and non-ischaemic LV dysfunction. Future studies will need to clarify if 3DSTE strain and CMR delayed contrast enhancement can provide incremental value to the prediction of future cardiovascular events.

     

Chronic fatigue syndrome in women assessed with combined cardiac magnetic resonance imaging

Objective

In chronic fatigue syndrome (CFS), only a few imaging and histopathological studies have previously assessed either cardiac dimensions/function or myocardial tissue, suggesting smaller left ventricular (LV) dimensions, LV wall motion abnormalities and occasionally viral persistence that may lead to cardiomyopathy. The present study with cardiac magnetic resonance (CMR) imaging is the first to use a contrast-enhanced approach to assess cardiac involvement, including tissue characterisation of the LV wall.

Methods

CMR measurements of 12 female CFS patients were compared with data of 36 age-matched, healthy female controls. With cine imaging, LV volumes, ejection fraction (EF), mass, and wall motion abnormalities were assessed. T2-weighted images were analysed for increased signal intensity, reflecting oedema (i.?e. inflammation). In addition, the presence of contrast enhancement, reflecting fibrosis (i.?e. myocardial damage), was analysed.

Results

When comparing CFS patients and healthy controls, LVEF (57.9 ± 4.3?% vs. 63.7 ± 3.7?%; p < 0.01), end-diastolic diameter (44 ± 3.7 mm vs. 49 ± 3.7 mm; p < 0.01), as well as body surface area corrected LV end-diastolic volume (77.5 ± 6.2 ml/m² vs. 86.0 ± 9.3 ml/m²; p < 0.01), stroke volume (44.9 ± 4.5 ml/m² vs. 54.9 ± 6.3 ml/m²; p < 0.001), and mass (39.8 ± 6.5 g/m² vs. 49.6 ± 7.1 g/m²; p = 0.02) were significantly lower in patients. Wall motion abnormalities were observed in four patients and contrast enhancement (fibrosis) in three; none of the controls showed wall motion abnormalities or contrast enhancement. None of the patients or controls showed increased signal intensity on the T2-weighted images.

Conclusion

In patients with CFS, CMR demonstrated lower LV dimensions and a mildly reduced LV function. The presence of myocardial fibrosis in some CFS patients suggests that CMR assessment of cardiac involvement is warranted as part of the scientific exploration, which may imply serial non-invasive examinations.

     

tBHQ和SFN在创伤性脑损伤小鼠中的疗效比较性分析

目的:探讨叔丁基对苯二酚(t BHQ)和莱菔硫烷(SFN)在患有创伤性脑损伤大鼠的疗效差异性。方法:80只健康成年的雄性SD大鼠分为假手术组、常规损伤组、t BHQ治疗组和SFN治疗组,使用电子颅脑损伤仪(e CCI)制备TBI模型。其中t BHQ治疗组在伤前24 h大鼠腹腔注射三次t BHQ(50 mg/kg),每8 h一次;SFN治疗组在伤后15 min给予腹腔注射SFN(5 mg/kg)。给药24 h后,采用m NSS方法评价各组大鼠神经功能缺损状况,利用干湿称量法计算脑含水量,Western blot和ELISA方法分别测定大鼠脑组织的NOX2和Nrf2的表达水平。结果:损伤发生后第24 h,t BHQ治疗组和SFN治疗组在m NSS评分((4.5±0.71)vs(9.2±0.79),(6.0±0.82)vs(9.2±0.79))、脑水肿(79.4%vs 85.6%,80.3%vs 85.6%)、NOX2和Nrf2(0.93 ng/m L vs 0.81 ng/m L,0.87 ng/m L vs 0.81 ng/m L)表达上与常规损伤组差异明显,而t BHQ治疗组和SFN治疗组间在m NSS评分((4.5±0.71)vs(6.0±0.82))、NOX2和Nrf2(0.93 ng/m L vs 0.87 ng/m L)表达上差异显著。结论:在大鼠TBI模型中,t BHQ和SFN均可以有效的降低机体自身的氧化应激作用,并改善神经功能,但t BHQ的疗效要好于SFN。     

n-6/n-3 多不饱和脂肪酸营养失衡对小鼠精子发生的影响

目的:探讨n-6/n-3多不饱和脂肪酸营养失衡对小鼠精子发生的影响。方法:健康的30只C57/B6雄鼠随机分为对照组(CON)、高脂组(HF)、花生四烯酸组(HF+AA)。喂食16周,做合笼实验并记录致孕率,通过精子动力分析仪检测小鼠精子活力和数量的变化,用Elisa试剂盒测血清中睾酮和甘油三酯水平。通过病理组织染色观察小鼠睾丸组织的形态学变化。利用Realtime-PCR的方法检测小鼠睾丸中Dazl基因表达水平的变化。结果:高脂组、花生四烯酸组与对照组相比精子活力[(16±0.01;12.33±2.83 vs72.2±12.73)%,P0.001],精子数量[(7.5±1.13;6±0.14 vs 13.87±0.35)million/m L,P0.001],致孕率[(28.57;14.29 vs 78.57)%,P0.001]及血清睾酮含量[(0.35±0.14;0.27±0.07 vs 3.51±0.7)ng/m L,P0.001]均显著性降低。高脂组、花生四烯酸组与对照组相比,血清中甘油三酯的含量显著增高[(0.74±0.04;0.74±0.04 vs 0.45±0.04)mmol/L,P0.001]。病理组织染色观察到花生四烯酸组小鼠睾丸组织出现了明显异形,曲细精管内部的初级精母细胞明显缺失,管腔中从初级精母细胞到精子的发生过程出现了变异,精子的数量也显著性下降。参与精子生成过程中的减数分裂前的有丝分裂增殖期、精原细胞的发育等过程的Dazl基因在高脂组和花生四烯酸组小鼠睾丸中的表达量与对照组相比显著降低(0.87±0.05;0.65±0.03 vs 1.07±0.04,P0.05)。结论:膳食中n-3/n-6多不饱和脂肪酸失衡会导致雄鼠精子发生发育的障碍     

Trimetazidine improves left ventricular function in diabetic patients with coronary artery disease: a double-blind placebo-controlled study

Background

Patients with diabetic cardiomyopathy have an impaired myocardial glucose handling and distal distribution of coronary atherosclerosis. Trimetazidine, an anti-ischemic metabolic agent, improves myocardial glucose utilization though inhibition of fatty acid oxidation. Aim of the present study was to evaluate whether the metabolic effect of trimetazidine on left ventricular function in patients with diabetic cardiomyopathy.

Methods

32 patients (24 males and 8 females, mean (SE) age = 67 ± 6 years) with type 2 diabetes and ischemic cardiomyopathy were randomized to receive either trimetazidine (20 mg, t.d.s.) or placebo (t.d.s.) for six months in a randomized parallel study. Patients performed an echocardiogram at baseline and after 6 months.

Results

Demographic data were comparable between the two groups. After six month baseline left ventricular end-diastolic diameters increased from 62.4 ± 1.7 to 63 ± 2.1 mm in the placebo group, while decreased from 63.2 ± 2.1 to 58 ± 1.6 mm (p < 0.01 compared to baseline) in the trimetazidine group. Compared to baseline, left ventricular ejection fraction increased by 5.4 ± 0.5% (p < 0.05) in the trimetazidine group while remained unchanged in the placebo group -2.4 ± 1.1% (NS), p < 0.01 between groups. A significant improvement in wall motion score index and in the E/A wave ratio was detected in patients treated with trimetazidine, but not in those receiving placebo.

Conclusion

in diabetic patients with ischemic heart disease trimetazidine added to standard medical therapy has beneficial effect on left ventricular volumes and on left ventricular ejection fraction compared to placebo. This effect may be related to the effect of trimetazidine upon cardiac glucose utilization.