川芎嗪对腹主动脉缩窄大鼠血浆醛固酮水平的影响

目的探讨川芎嗪对腹主动脉缩窄大鼠血浆醛固酮（ALD）水平的干预作用。方法银夹法建立腹主动脉缩窄大鼠模型,用放免法检测血浆ALD水平,观察川芎嗪对大鼠左室心肌质量指数（LVMI）、胶原染色和血浆ALD改变的干预作用。结果造模8W时,模型组LVMI和血浆ALD水平较假手术组显著升高（P〈0．01）;川芎嗪组较模型组显著降低（P〈0．01）,但与假手术组相比无明显变化（P〉0．05）。结论腹主动脉缩窄大鼠可发生心肌纤维化,血浆ALD水平升高,川芎嗪可延缓心肌的纤维化进程。     

组织应变成像技术对儿童主动脉缩窄左心功能的评价

目的:探讨组织应变成像技术在评价儿童主动脉缩窄患者手术治疗前后左心功能的临床应用价值.方法:24例主动脉缩窄患儿于手术前后接受常规超声及组织多普勒检测,获取二尖瓣血流E/A值、左室短轴缩短率(FS)、射血分数(EF)及左室心肌的收缩期及舒张早期峰值应变和应变率.结果:①患儿手术前后E/A值、FS及EF无明显差异(P＞0.05);②患儿收缩期峰值应变术前高于术后但无明显差异(P＞0.05).③患儿术后收缩期峰值应变率略低于术前(P＞0.05),舒张早期应变率峰值高于术前(P＜0.02).结论:应变及应变率可以敏感检测主动脉缩窄儿童术后左心功能的改善.     

葡萄糖“糖酵解-有氧氧化脱耦联”在慢性心肌肥厚进展中的作用

目的 探讨葡萄糖“糖酵解-有氧氧化脱耦联”在慢性心肌肥厚进展过程中的作用及其机制.方法 采用小鼠主动脉缩窄(TAC)模型诱导慢性心肌肥厚至慢性心力衰竭过程.采用Western blotting检测慢性心力衰竭进展过程中磷酸化丙酮酸脱氢酶(p-PDH)蛋白的动态表达变化,同时观察DCA药物处理对小鼠心功能及生存曲线的影响;采用TUNEL法原位检测两组心肌细胞凋亡的改变.结果 Western blotting结果表明,小鼠TAC模型中p-PDH的表达在术后第1天即开始升高,术后第3天达到峰值,术后2周仍升高,而在术后12周时表达很低.与对照组相比,DCA处理组的p-PDH明显降低(P＜0.05);进一步超声心功能分析表明,DCA处理组加速了失代偿期心功能的恶化,进而降低了小鼠的20周生存率;TUNEL法半定量分析结果显示,DCA处理组的心肌细胞凋亡指数(29.3±2.5)明显高于对照组(18.8±1.9,P＜0.05).结论 心肌的葡萄糖代谢从糖酵解向氧化磷酸化转变促进了代偿性心肌肥厚向失代偿性心力衰竭的转变;葡萄糖氧化磷酸化促进心力衰竭的机制与心肌细胞凋亡增多有关.     

腹主动脉缩窄大鼠模型心肌Ⅰ型和Ⅲ型胶原改变及其mRNA的表达

目的:通过建立腹主动脉缩窄大鼠模型,观察腹主动脉缩窄大鼠心肌中Ⅰ型、Ⅲ型胶原及其mRNA的表达.方法:30只雄性SD大鼠随机分为假手术组(14只)和模型组(16只).模型组根据Doering等的方法,用银夹造成腹主动脉部分狭窄(银夹内径0.7 mm).8 w后用免疫组化法对心肌组织Ⅰ型和Ⅲ型胶原染色,并用光密度值作为其含量指标行图像分析,即时PCR扩增后分析并测定胶原mRNA水平.结果:模型组造模8 w时,Ⅰ型和Ⅲ型胶原平均光密度及其mRNA表达较假手术组显著升高(P＜0.01).胶原组化染色显示,模型组胶原明显增多、增粗、排列紊乱.结论:大鼠腹主动脉缩窄导致反应性纤维化心肌中Ⅰ型和Ⅲ型胶原及其mRNA表达升高,以心肌间质和血管周围增加为主;本模型适合高血压、心力衰竭等慢性过程致心肌纤维化的研究.     

彩色M型多普勒评价室壁肥厚患者左室舒张功能的临床研究

目的：探讨应用M型彩色多普勒评价室壁肥厚患者左室舒张功能的临床价值。方法：研究32例左室肥厚患者，包括肥厚型心脏病（HCM）10例、高血压性心脏病（HHD）Ⅱ期左室肥厚22例，正常对照（NC）20例，分别测量左室舒张早期血流播散速度（Vp）、E峰与Vp的比值（E／Vp）等指标。结果：室壁肥厚患者不论E／A〉1，还是E／A〈1，其Vp和E／Vp与对照值相比，均有显著性差异（P〈0．01）。结论：彩色M型多普勒无“假性正常化”现象，是评价左室舒张功能的可靠指标。     

超声心动图对左房室瓣球囊扩张术后左室心肌重量及心脏收缩功能变化的评价

目的　应用经胸超声心动图(UCG)评价皮穿刺左房室瓣球囊扩张术对风湿性左房室瓣狭窄患者的左室心肌重量和心脏收缩功能的影响。方法　使用美国Agilent公司生产的PhilipsSonos 5 5 0 0、75 0 0型彩色多普勒超声心动图仪检测4 0例风湿性左房室瓣狭窄患者成功行皮穿刺左房室瓣球囊扩张术后的左室心肌重量、左室收缩功能及左室内径大小的变化,分别于经皮穿刺左房室瓣球囊扩张术术后3d内和手术后3个月接受超声心动图检查。所有研究对象均进行经胸M型、二维及多普勒超声心动图检查,采用二维超声心动图根据面积-长度法测量左室心肌重量,并与体表面积换算成左室心肌重量指数;M型超声心动图测量左室舒张末期径以及根据Teichholz校正公式测量左室射血分数(EF)、左室短轴缩短率(FS)、每搏出量(SV)和心输出量(CO) ;二维及多普勒超声心动图分别按椭圆形面积公式及压差半降时间(pressurehalftime ,PHT)法测量左房室瓣口面积(MVA)。结果　(1)经皮穿刺左房室瓣球囊扩张术后3d全部患者的左室舒张末期径增大(P <0 .0 1) ;射血分数(EF)、左室短轴缩短率(FS)、每搏出量(SV)和心输出量(CO)均明显提高(P <0 .0 0 1) ;同时室间隔厚度、左室后壁厚度、左室心肌重量和左室心肌重量指数也有所改变(P <0 .0 5 ) ;(2 )术后3个月室间     

肥厚型心肌病之不常见胸部X线所见

肥厚型心肌病亦称左室功能性梗阻,非对称性间隔肥厚,特发性肥厚性主动脉下狭窄,肌性主动脉下狭窄等。系左室(有时亦可累及右室)心肌的不一致性肥厚。本病引起血液动力学及心电图变化现已逐渐为人所知。心肌纤维的排列紊乱与纤维化     

吡那地尔对压力负荷性心力衰竭大鼠心肌重塑的影响

目的探讨吡那地尔对压力负荷性心力衰竭大鼠心功能及心肌重塑的影响。方法腹主动脉缩窄法建立大鼠压力负荷性心力衰竭模型,40只雄性Wistar大鼠随机分为假手术组（n=10）、手术组（n=20）和吡那地尔组（n=10）。吡那地尔组大鼠从术后4周开始应用KATP开放剂吡那地尔2mg·kg-1·d-1治疗。术后第12周行血流动力学检测动脉收缩压、舒张压,左室内压上升下降最大速率（±dp/dtmax）和左室舒张末压（LVDEP）。酶联免疫吸附法（ELISA）测定血清B型脑钠肽（BNP）、I型胶原和Ⅲ型前胶原氨基末端肽（PⅢNP）浓度。处死大鼠后称量心脏质量,计算心脏重量指数（心脏质量/体质量）。HE染色计算心肌纤维直径。结果①手术组大鼠心脏重量指数和心肌纤维直径均明显升高,吡那地尔组均显著降低;②手术组收缩压、舒张压、LVEDP明显升高,吡那地尔组明显降低;±dp/dtmax在手术组明显降低（P〈0.01）。手术组血清BNP水平明显升高,吡那地尔组虽然也降低,但仍高于假手术组（P〈0.01）;③手术组I型胶原和PⅢNP的血清浓度明显大于假手术组。吡那地尔组均明显降低（P〈0.01）。结论吡那地尔可改善大鼠腹主动脉缩窄术后的心脏肥厚和心肌纤维化,延缓心力衰竭的进展。     

超声心动图定量评价冠脉支架置入术后左室收缩功能变化

目的:应用组织多普勒成像(DTI)及主动脉瓣上流速定量评价冠状动脉置入术后左室局部及整体收缩功能的变化,旨在探讨超声心动图评价冠状动脉支架置入术后左室收缩功能改善情况的简便方法.方法:采用PW-DTI技术对59例急性心肌梗死并行冠状动脉支架置入术患者分别干术前24h、5d、15d检测左室梗死区对应心肌节段的基底段、中段心肌的收缩期峰值速度PSV,比较支架置入前后梗死区局部心肌收缩速度变化;同时检测支架置入术前后主动脉瓣上血流速度变化,记录并测量支架置入前后左室射血分数LVEF的变化.结果:术后5d左室受累节段心肌收缩期峰值速度较术前明显增加,P＜0.05;术后15d受累节段心肌收缩期峰值速度较术前及术后5d均明显增加,P＜0.01;术后5d主动脉瓣上流速较术前增加,P＜0.05,术后15d主动脉瓣上流速较术前及术后5d均显著增加,P＜0.01;术后5d LVEF较术前有增加趋势,但差异无统计学意义,术后15dLVEF较术前明显增加,差异有统计学意义,P＜0.01.结论:冠状动脉支架置入术后早期左室局部心肌收缩功能有明显改善,随时间延长心肌收缩功能显著提高,组织多普勒成像可直观、定量估测受累心肌恢复情况;主动脉瓣上流速亦可直观评估左室整体收缩功能改善情况,流速变化较组织多普勒及左心功能测定更加直观简便.     

科素亚对轻中度原发性高血压左室肥厚的逆转作用

 目的 观察科素亚对轻中度原发性高血压左室肥厚的逆转作用.方法 采用自身对照试验,对64例轻中度原发性高血压左室肥厚的患者,用科素亚50～100 mg/d治疗,共12周,随访患者血压、超声心动图变化以及服药耐受性.结果 12周后,所有患者血压均较入院时明显下降(P＜0.05),室间隔厚度(IVST)、心室后壁厚度(PWT)、左室重指数(LVMI)均有明显减少(均为 P＜0.01),说明左室肥厚减轻,左室舒张功能得到改善,且无明显不良反应.结论 科素亚有确切降压效果,并有逆转左室肥厚的作用.     

Angiotensin II inhibition attenuates postexercise proteinuria in rats

An important explanatory theory for the mechanism of postexercise proteinuria is that angiotensin II could be inhibited by angiotensin converting enzyme inhibitors. Because of the kininase effect of the angiotensin converting enzyme, it is unclear whether the kallikrein-kinin system contributes to the effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. The aim of this study was to evaluate any possible involvement of the kallikrein-kinin system in the therapeutic effect of angiotensin converting enzyme inhibitors on postexercise proteinuria. We evaluated urinary protein levels in exhausted rats receiving an angiotensin converting enzyme inhibitor (enalapril) or an angiotensin II type I receptor antagonist (losartan). Enalapril (30 mg/kg/day, two days) or losartan (20 mg/kg/day, two days) were given to animals using an intragastric catheter. Urinary protein levels increased (41 %) in rats which were exhausted via treadmill running (p < 0.05). In animals that received drug treatment (enalapril or losartan), but did not exercise to exhaustion, urinary protein levels were not different from the control group. Urinary protein levels were found to be significantly lower (p < 0.05) in animals which performed acute exhaustive exercise after enalapril or losartan administration, compared to rats which were exhausted without drug administration. Inhibition of postexercise proteinuria by either enalapril or losartan suggested that angiotensin II plays an important role in postexercise proteinuria, however, it appears the kallikrein-kinin system is not involved in angiotensin converting enzyme inhibitors effect.     

卡维地洛联合科素亚对高血压患者左室结构及功能的影响

 目的观察卡维地洛联合科素亚对高血压病(EH)患者左室结构及功能的影响.方法观察84例高血压患者口服卡维地洛联合科素亚平均12个月后左室结构和功能改变.治疗前及治疗后12个月分别进行心脏超声检查,测量有关心血管参数.结果治疗后降压效果显著(P＜0.01),室间隔(IVST)、左室后壁(PWT)及左室重量指数(LVMI)均明显下降(P＜0.01),A峰速度明显下降,E峰速度及E/A比值明显增高(P＜0.01).结论卡维地洛联合科素亚治疗高血压病可安全有效降压,并同时逆转左室肥厚,改善左室舒张功能.     

运动性心肌肥大大鼠心肌肌肉生长抑制素表达的变化

目的:观察运动性心肌肥大大鼠心肌组织肌肉生长抑制素(myostatin,MSTN)表达的变化。方法:16周龄雄性SD大鼠随机分为对照组和运动组,每组10只。运动组进行持续8周跑台训练,每周5次,每次60分钟,跑速26米/分钟。测定两组大鼠心重并计算心系数,HE染色观察心肌细胞横截面积,分别采用real-time PCR技术和western blot方法测定心肌MSTN mRNA和蛋白表达,放免法测定血浆MSTN水平。结果:运动组大鼠心脏重量和心系数显著高于对照组(P<0.05),心肌细胞横截面积增大。运动组大鼠血浆MSTN水平、心肌MSTN mRNA和蛋白表达显著低于对照组(P<0.05)。结论:运动性心肌肥大时,大鼠心肌MSTN mRNA和蛋白表达被抑制,可能通过解除其对心肌生长的负调控作用,促进心肌细胞对运动产生适应性肥大。     

运动性心肌肥大大鼠背根神经节降钙素基因相关肽基因表达的变化

目的:探讨运动性心肌肥大大鼠背根神经节降钙素基因相关肽基因表达的变化。方法:雄性SD大鼠随机分为对照组(n=33)和耐力训练组(n=33)。耐力训练组进行10周的跑台耐力训练,建立运动性心肌肥大模型。建模后48h,从两组随机抽取17只大鼠,连续3天进行力竭运动,最后一次力竭运动后即刻处死全部实验动物。记录力竭运动距离和大鼠体重,取大鼠心脏和腰段背根神经节,记录心脏湿重,采用荧光定量聚合酶链式反应技术测定大鼠背根神经节降钙素基因相关肽mRNA的表达量。结果:10周后,耐力训练组大鼠心脏重量与体重之比和力竭运动距离显著高于对照组(P<0.01)。与对照组比较,力竭运动前耐力训练组背根神经节CGRPmRNA表达显著下降(P<0.01),力竭运动后耐力训练组背根神经节CGRPmRNA表达与力竭运动前相比无明显变化,而对照组较力竭运动前显著下降(P<0.01)。结论:运动性心肌肥大大鼠背根神经节CGRP基因表达下调,力竭运动后表达保持稳定。     

Cyclosporin A does not block exercise-induced cardiac hypertrophy

Cyclosporin A (CsA) has been shown to inhibit pathophysiological models of overload-induced cardiac hypertrophy, indicating a role for the calcium dependent signal pathways. It is unclear what impact CsA may have on the myocardial response to exercise, a physiological model of overload.PURPOSE: The purpose of the study was to determine whether CsA would alter exercise-induced cardiac hypertrophy. METHODS: Thirty male rats were assigned to vehicle or CsA injection (15 mg.kg.d(-1)) and then assigned to sedentary or exercise training. Animals were swum for 60 min.d(-1) for 1 wk. RESULTS: One week of swim training significantly increased plantaris cytochrome oxidase activity, as well as significantly increasing left ventricular (LV) weight and the left ventricular:body weight (LV/BW) ratio. Exercise did not alter right ventricular (RV) weight or the RV/BW ratio. RNA analysis found that exercise significantly increased atrial natriuretic factor (ANF)-mRNA levels but did not influence alpha-myosin heavy chain (MHC) expression. CsA treatment, but not exercise, was associated with a significant increase in betaMHC expression. Western blot analysis determined that betaMHC protein was also significantly increased in the CsA-treated animals. CONCLUSION: CsA did not block exercise-induced cardiac hypertrophy but did significantly influence the myocardial phenotype. The CsA-sensitive calcium dependent pathways, important for pathological forms of overload-induced hypertrophy, were not essential to the early adaptations to exercise and that a different mechanism or signal transduction pathway was engaged. The data also indicate that CsA alone may induce a shift in the MHC isoform expression toward that associated with a pathological phenotype. Whether this phenotype shift contributes to the lowered exercise capacity found in transplant patients remains to be determined.     

卡托普利对缺氧大鼠心肌血管紧张素Ⅱ含量及右心室肥大的影响

观察了间断性缺氧大鼠血浆与右心室血管紧张素Ⅱ（AugⅡ）含量、右心室超微结构的变化及卡托普利对缺氧性右心室肥大的影响。结果表明，慢性缺氧引起右心室收缩压升高，右心室AugⅡ含量及右心室重量指数增加，心肌线粒体及肌原纤维变性。服用卡托普利后右心室收缩压、右心室重量指数和AugⅡ含量降低，心肌超微结构接近正常。说明AngⅡ在缺氧性右心室肥大发生中起着重要作用。     

c-fos和c-myc 原癌基因与bFGF在烧伤后早期创面组织中的表达规律

目的：探讨烧伤后创面组织原癌基因ｃ－ｆｏｓ、ｃ－ ｍｙｃ 和碱性成纤维细胞生长因子（ｂＦＧＦ） 的表达顺序及分布规律。方法：采用深Ⅱ度烫伤模型,将４２ 只大鼠分为７ 组,即正常对照组、烫伤后３ ｈ、６ ｈ、１ ｄ、３ ｄ、７ ｄ 和１４ ｄ 组。用ＳＰ免疫组化方法研究烫伤后不同时间点内源性ｃ－ｆｏｓ、ｃ－ ｍｙｃ 和ｂＦＧＦ蛋白的表达规律及分布特征。结果：烧伤可以诱导ｃ－ｆｏｓ、ｃ－ ｍｙｃ 和ｂＦＧＦ表达,但三者的表达模式不尽相同,正常皮肤即有ｃ－ｆｏｓ 表达,伤后３ ｈ 达峰值,以后逐渐下降,１ 天以后降至最低水平,其阳性颗粒主要分布于表皮基底细胞胞浆及真皮成纤维细胞的胞核内。ｃ－ ｍｙｃ 的表达在伤后３ 天达最高值,阳性信号分布于真皮层成纤维细胞的胞浆中;而ｂＦＧＦ则在伤后６ ｈ 开始出现,伤后第１ 天达最高值,主要分布于真皮层的成纤维细胞的胞浆中。结论：烧伤可以诱导皮肤创面组织原癌基因ｃ－ｆｏｓ、ｃ－ ｍｙｃ 及ｂＦＧＦ的表达,其表达具有时相与部位分布特征。三者表达的时相性提示在烧伤后早期原癌基因与生长因子基因之间具有相互调控作用,而这种调控作用对后期组织修复将产生一定的影响。     

耐力训练过程中大鼠心肌组织心钠素、脑钠素基因的表达

本研究采用定量反转录聚合酶链式反应技术,观察大鼠在11周中等强度耐力训练过程中心肌心钠素(ANP)和脑钠素(BNP)基因表达的变化.结果显示,大鼠心室BNP mRNA表达在训练第24天、第3天和第77天均较对照组显著增强(P＜0.01),心房BNP mRNA表达无显著变化.大鼠训练第38天,心室ANP mRNA表达显著高于对照组(P＜0.01),其余各时相较对照组变化不明显,训练第3天心房ANP mRNA表达显著高于对照组(P＜0.01),其余各时相较对照组变化不明显.结论:在耐力训练过程中,心肌BNP基因表达与ANP不一致,心室BNP基因表达变化与心肌肥大的发展过程一致,提示BNP在运动性心肌肥大发展过程中起着一定的作用.     

Losartan renography for the detection of renal artery stenosis: comparison with captopril renography and evaluation of dose and timing

Purpose Radionuclide renography with angiotensin converting enzyme (ACE) inhibition plays an important role in the diagnosis of haemodynamically significant renal artery stenosis. Angiotensin receptor antagonists inhibit the renin angiotensin system at different levels from ACE inhibitors by selectively blocking the binding of angiotensin II to AT1 receptors. The AT1 angiotensin receptor antagonist losartan has recently been used clinically in the treatment of hypertension. However, the available data on the use of losartan with renography for the detection of renovascular hypertension are limited and contradictory. The purpose of this prospective study was to compare the effectiveness of losartan renography and captopril scintigraphy in revealing renal artery stenosis.Methods A total of 61 renal units in 32 patients with hypertension were studied in two groups based on the losartan dosage (50 mg in group A and 100 mg in group B). Group A consisted of 17 patients, in whom 19 renal units had angiographically proven renal artery stenosis (50%). In group B, there were 15 patients, in whom 20 renal arteries were stenotic. All of the patients underwent three renographies (baseline, captopril renography and early losartan renography). Early losartan renography was performed at 1 h after oral losartan administration in both groups. In group B, seven patients underwent additional losartan renography (late losartan) performed 3 h after oral losartan administration; these patients composed group B1.Results The sensitivities of captopril and losartan studies were 63.2% and 42% in group A, 65% and 65% in group B and 55.6% and 66.6% in group B1, respectively.Conclusion From our preliminary results, we conclude that losartan is not superior to captopril renography for the detection of haemodynamically significant renal artery stenosis. However, a high dose (100 mg) of losartan provided higher sensitivity than the lower dose (50 mg). Late losartan scintigraphy provided similar diagnostic efficacy to early losartan renography.This work was presented as an abstract at the Annual Congress of the EANM, Helsinki, 2004.     

血管紧张素Ⅱ在运动性心肌肥大中的作用

为探讨心脏局部ＡｎｇⅡ在运动性心肌肥大中的作用，本文在长期游泳训练造成的心肌肥大模型上观察心脏系数、心肌局部和血浆ＡｎｇⅡ含量的变化，同时观察应用转换酶抑制剂Ｃａｐｔｏｐｒｉｌ对心肌肥大的心脏系数及心肌和血浆ＡｎｇⅡ含量的影响。结果表明，运动可引起左右室心肌肥大，左右室心脏系数较对照组分别增加了１９％和２３．４％，这种心肌局部肥大和血浆ＡｎｇⅡ的含量较对照组分别增加了４８．３％和４４．５％（ｐ＜０．０１），应用Ｃａｐｔｏｐｒｉｌ可阻断运动性心肌肥大的发生，左右室系数较单纯运动心肌肥大组分别降低了１８．２％和１７．８％且血浆和心肌局部ＡｎｇⅡ的含量较单纯运动心肌肥大组分别降低了５８％和５５．８％（ｐ＜０．０１），相关分析结果提示，心肌局部ＡｎｇⅡ的含量与心肌肥大的程度成显著正相关（ｒ＝０．６６５ｐ＝０．０１３），由此证明心肌局部ＡｎｇⅡ参与了运动性心肌肥大的发生过程。