心肌弹性的实验研究(二)

心脏的收缩和舒张功能与心肌弹性密切相关。为了研究心肌的弹性，探讨心衰的机理，作者对离体猪心的弹性模量进行了测试，实验结果表明，心肌的弹性优于骨骼肌、血管和腱。     

诱发交替脉的心率与左室功能的关系

临床上交替脉是心脏重度衰竭的征象。实验研究常用心脏快速起搏诱发交替脉,并已发现,只要起搏频率足够快,正常功能的心脏亦可产生交替脉。为探     

还少丹对D-半乳糖致衰小鼠心肌线粒体结构与功能的影响

目的:探讨还少丹对D-半乳糖(D-galactose,D-gal)诱导的衰老模型小鼠心肌线粒体结构与功能的影响.方法:将小鼠随机分为空白对照组、衰老模型组、还少丹低、高剂量组.采用D-gal建立衰老模型,还少丹水煎液灌胃6周.以差速离心法分离小鼠心肌组织线粒体;Comas亮蓝蛋白定量法测定线粒体蛋白含量;分光光度法检测...     

心肌局部冷冻后形态和功能的变化

目的：观察心肌局部冷冻后形态和功能变化。方法：实验动物随机分成实验组和对照组；在实验组中，利用冷冻探头(—60℃)对心肌进行局部冷冻，用温的生理盐水复温。研究心脏输出功能、心脏电生理、生化以及组织学变化。结果：急性期可见到心肌呈炎性改变，远期可见到疤痕形成；冷冻前后、心电因、电解质以及心室舒张、收缩压未见变化；心肌酶谱各项酶明显升高。结论：心肌冷冻是安全的；疤痕形成可能是心肌传导阻滞的原因之一。     

低氧和低氧游泳大鼠心肌糖原含量与右室功能的变化

目的：观察慢性低氧及低氧游泳大鼠心肌糖原含量的变化，探讨其与右心舒缩功能升降的关系。方法：采用低压舱模拟海拔5000 m连续低氧及低氧游泳大鼠模型，用比色法测定其心肌糖原含量；用右心导管法经RM-6000生理多导记录仪记录右心舒缩功能指标。结果：大鼠心肌糖原含量在低氧早期即显著下降，随低氧时间的延长，呈较明显进一步下降的趋势，而右心功能则逐渐增强；低氧游泳组大鼠右心功能明显增强，其心肌糖原含量接近平原对照水平，显著高于单纯低氧组。结论：大鼠在低氧条件下适量作功（游泳），可能有利于机体的低氧适应。     

美心力对左室功能和血流动力学影响的实验研究

目的：探讨美心力（cAMP)对左室功能和血流动力学的影响。方法：建立心内植入压力、容积测定装置的犬模型。利用压力-容积关系分析美心力对左室功能和血流动力学的影响。结果：美心力明显减慢心率（HR）,降低总外周阻力（TSR）,使左室收缩末期压力（PES）、容积（VES）和舒张末期压力（PED）、容积（VED）明显下降;并加速左室舒张速度（Tc),使每搏容积（SV）及射血分数（EF）增加,对于左室PES-VES、左室压上升最大速率（dp/dtmax)-VED和心搏功（SW）-VED3种关系斜率及位置无影响。表明无正性肌力作用。结论：美心力无正性肌力作用。但能够降低心脏负荷,改善心肌舒张功能,增加心排血量。     

B10细胞减缓病毒性心肌炎诱导的心肌肥厚的机制研究

目的:探讨心肌炎后B10细胞参与心肌细胞肥大的机制,为预防心肌炎诱导的心肌肥大探寻潜在的治疗策略。方法:体内实验选取柯萨奇病毒B3感染BALB/c小鼠诱导的病毒性心肌炎模型,检测心脏肥大相关指标,检测心肌炎小鼠血管紧张素Ⅱ及其受体表达量,流式分析对照组小鼠以及心肌炎小鼠心脏中B10细胞的改变。氯沙坦灌胃心肌炎小鼠后,苏...     

高血压无左室肥厚患者舒张功能改变的观察

目的：探讨高血压无左室肥厚患者舒张功能的改变。方法：高血压无左室肥厚患者、高血压伴左室肥厚患者与正常血压者各４０例,均进行超声心动图检查和动态血压检测。结果：高血压伴左室肥厚组、高血压无左室肥厚组与正常对照组比较,二尖瓣血流Ｅ峰、Ａ峰、Ｅ／Ａ比率、等容舒张时间及舒张早期减速度均有明显差异（Ｐ＜００５,Ｐ＜００１）,而高血压左室肥厚组与高血压无左室肥厚组两组间,则无明显差异（Ｐ＞００５）。３个组的左室射血分数（ＥＦ）无明显差异（Ｐ＞００５）。动态血压监测显示,高血压左室肥厚组与高血压无左室肥厚组２４ｈ平均收缩压和舒张压、白昼平均收缩压和舒张压、血压负荷有显著差异（Ｐ＜００５,Ｐ＜０．０１）,而夜间平均收缩压、舒张压无显著差异（Ｐ＞００５）。结论：高血压患者在出现左室肥厚前可出现舒张功能异常,可能与夜间血压持续升高有关。     

实验性心肌肥厚大鼠血浆与心肌儿茶酚胺含量变化及黄芪的影响

结扎大鼠腹主动脉形成实验性心肌肥厚，对动物血浆及左心室组织中肾上腺素、去甲肾上腺素含量与心肌肥厚程度，以及黄芪注射液和卡托普利抗肥厚作用之间的相关性进行研究。手术4周后开始连续给药8周。以动物的心脏重量衡量心肌肥厚程度，用HPLC法测定血浆及左心室组织中肾上腺素和去甲肾上腺素含量，以SPSS统计软件对二者的相关性进行分析。结果显示模型组动物肾上腺素在血浆和心室组织中的含量均比对照组升高，去甲肾上腺素的血浆浓度比对照组升高，而其左心室组织中含量则低于对照组。黄芪注射液和卡托普利有不同程度的抗心肌肥厚作用，并可部分纠正肾上腺素和去甲肾上腺素含量的异常变化。相关性分析结果显示，心肌肥厚程度（全心重量、左心室重量）与左心室组织中去甲肾上腺素含量呈显著负相关性（P＜0．01）。上述结果提示：药物改变体内儿茶酚胺类物质含量可在一定程度上反映药物对心肌肥厚程度的影响。     

Evaluation of left ventricular function during ejection

Several ejection indices of left ventricular performance are described. The most sensitive is the rate of change of power, especially when measured at the time of peak left ventricular wall tension. When measured at peak tension, the rate of change of power reflects force-velocity-length relations and, therefore, is theoretically appealing. The rate of change of power itself incorporates terms shown to be of functional significance. Among these is the rate of change of flow. This expression is more readily measured than the rate of change of power and can be approximated noninvasively by the measurement of blood acceleration.     

一氧化氮合酶2抑制剂对大鼠心肌梗死后左心室形态及心功能的影响

目的：观察选择性一氧化氮合酶2（NOS2）抑制剂S-甲基硫脲（SMT）对心肌梗死（MI）后左心室形态学和血流动力学指标的影响，探讨NOS2在MI后心功能障碍形成过程中的作用。方法： 于大鼠冠状动脉结扎前30 min给予SMT灌胃，6周后测定左心室形态学和血流动力学指标、心肌NOS2表达量、血浆NO2-/NO3-水平、心肌纤维化程度。结果： MI后6周，心脏非梗死区NOS2表达量、血浆NO2-/NO3-水平、中心静脉压和左室舒张末压高于对照组。使用SMT可降低血浆NO2-/NO3-水平［(26.6±6.1） μmol/L vs （50.1±10.4） μmol/L, P＜0.01］，减少心肌梗死范围（36.0%±7.2% vs 42.6%±8.6%, P＜0.05），减轻心室扩张［LVD，（6.6±0.3） mm vs （7.2±0.3） mm, P＜0.01］，减小心肌细胞直径［(15.1±1.6） μm vs （16.9±2.3） μm, P＜0.05］，减轻心肌纤维化［CVF，4.1%±1.1% vs 5.7%±1.2%, P＜0.01］，降低中心静脉压［（0.9±0.3） mmHg vs （1.5±0.5） mmHg, P＜0.01］和左室舒张末压［（8.1±2.4） mmHg vs（13.4±3.1） mmHg, P＜0.01］，提高存活率（72.4% vs 39.3%, P＜0.05）。结论： 大鼠MI后，NOS2可能起促进心功能障碍形成的作用。抑制NOS2可以减轻心室重构，改善心功能。     

高血压性左室肥厚患者的校正QT间期离散度变化及临床意义

目的：研究高血压性左室肥厚患者的ＱＴｃｄｅ变化及临床意义。方法;采用１２导联心电图同步记录,超声检查一动态心电图监测５６例高血压患者的ＱＴｃｄ,心脏形态和心律失常。结果：高血压病组和对照组间ＱＴｃｄ差异非常显著,高血压伴ＬＶＨ组和室性心律失常组的ＱＴｃｄ均显著长于无伴ＬＶＨ组和或无ＶＡｓ组;ＬＶＨ组ＶＡｓ和复杂型心律失常发生率均显著高于无ＬＶＨ组。     

Coronary perfusion pressure and left ventricular function

Summary A stable preparation is described in which the left ventricle is functionally siolated from the rest of the circulation of dogs. Mean aortic (MAP) and mean left atrial pressures (MLAP) can be varied independently while aortic flow (AF) is measured as a dependent variable. Experimental studies showed that when MLAP was kept constant and MAP was varied, a definite maximum of AF was obtained at a MAP that varied widely fromanimal to animal between 36 and 98 mm Hg. The value of MAP where this maximum AF was found increased on the average 10 mm Hg for each increase in maximum AF of 1 l/min.To facilitate comparison of the results obtained under different conditions and from different animals, the value of MAP at which a maximum AF was found equal, to 100 ml/min x kg was determined from the results of each experiment and defined as Optimum MAP. The Optimum MAP was found to be higher at higher heart rates: a linear relationship was observed indicating an increase of approximately 0.36 mm Hg per increase in heart rate of 1 BPM. Lowering the hematocrit in the range between 43 and 24 percent resulted in a decrease of the Optimum MAP, with a minimum between 20 and 24 percent; below 20 percent the Optimum MAP increased with a further decrease of hematocrit.Distinction is made between myocardial oxygen consumption and oxygen supply and equations are derived that relate these quantities with MAP, AF, heart rate and hematocrit.It is suggested that the Optimum MAP is closely associated with the lower limit of the autoregulation range of coronary flow.This work was supported by grants-in-aid from the USPHS (HE-08375 and HE-10581) and from the American Heart Association (65-G-95). Dr.Beneken was an International Postdoctoral Research Fellow from the USPHS (FO5-TW-1133-01), on leave from the Institute of Medical Physics TNO, Utrecht, The Netherlands.     

儿童房间隔缺损封堵术前后血液动力学及心功能的研究

目的:评价儿童房间隔缺损(ASD)封堵术前后的血液动力学及左心功能改变。方法:应用Amplatzer封堵器成功施行经皮股静脉穿刺ASD封堵术患儿10例, 于术前、术后48h、3个月及6个月行超声心动图检查。左心室容积采用面积长度法计算;左心室几何构型采用偏心率及左心室长径/短径比值评价。结果:ASD封堵术后48h, 左心室舒张末期前后径、舒张末期容积增大、每搏量、射血分数及短轴缩短率增大, 左心室偏心率及长径/短径比值缩小(P＜0.05);左心室前负荷、收缩功能及几何构型在短、中期随访中持续改善。术后及短、中期随访中左心室晚期充盈分数, 差异无显著(P＞0.05)。结论:ASD封堵术不仅根治了先天性解剖畸形, 纠正了血液动力学异常, 也改善了左心室收缩功能及几何构型, 在短、中期随访中, 左心室功能及几何构型持续改善。     

Parameters of ventricular contractility in mice: influence of load and sensitivity to changes in inotropic state

We examined the relative usefulness of parameters to determine left ventricular contractility in mice invasively. The optimal parameter must be sensitive to changes in inotropy and insensitive to changes in loading. Furthermore, it should be able to confirm or reject the hypothesis of altered myocardial contractility after a limited number of experiments. Left ventricular function was assessed in closed-chest mice using a microtip pressure-conductance catheter at baseline and after increases in preload, afterload, or contractility. The parameters are differentially influenced by loading conditions and inotropic state. Only those parameters that could differentiate between basal and increased contractility with a power of 0.85 in ten or less experiments were considered useful. Ejection fraction, preload-recruitable stroke work (PRSW), and dP/dt_max/V _ed could demonstrate the smallest changes in contractility. Stroke work, maximal power and dP/dt_max were most influenced by preload. End-systolic elastance, ejection fraction, and stroke work were afterload-dependent. Dividing the magnitude of the effect of inotropic stimulation to that of load changes gives an index for the usefulness for each parameter. A high ratio indicates that the change in parameter reflects inotropic rather than load change. This ratio was highest for PRSW, which seems to be the best parameter for judging contractility differences in mice.     

短时高强度间歇运动训练心肌梗死模型大鼠心室重构及线粒体变化

BACKGROUND: It is unclear whether short-term high-intensity interval training (HIT) can be used to protect against myocardium injury after acute myocardial infarction, as well as the underlying mechanism.     

rAAV-mediated angiogenin gene transfer induces angiogenesis and modifies left ventricular remodeling in rats with myocardial infarction

In vitro studies have demonstrated that bovine angiogenin (ANG) significantly stimulates both the migration of endothelial cells and the formation of tubelike structures. The aim of this study was to explore whether ANG gene transfer could enhance vascularization, modify left ventricular remodeling, and attenuate cardiac dysfunction in rats with myocardial infarction (MI). We constructed a recombinant adeno-associated virus vector encoding the ANG gene (rAAV-ANG) and evaluated its angiogenic potential after regional transfection by intramyocardial injection immediately after left anterior descending artery ligation in rats. Four weeks after coronary artery ligation, rAAV-ANG transfection upregulated the myocardium ANG protein expression level in both normal and MI rats, and immunohistochemistry showed that the overexpressed ANG was distributed in the cytoplasm of cardiomyocytes. In rats with MI, rAAV-ANG treatment altered left ventricular remodeling, as indicated by a decrease in left ventricular end diastolic diameter, left ventricular end systolic diameter, cardiomyocyte diameter, ventricular weight to body weight ratio and interstitial fibrosis infiltration. We also found an increase in capillary density and partly restored cardiac function in the group receiving rAAV-ANG treatment. These results confirmed that in rats with MI, ANG gene transfer could induce angiogenesis, alter left ventricular remodeling, and attenuate cardiac dysfunction. This study provides a new choice of treatment for ischemic heart disease.     

中西药结合逆转高血压左心室肥厚及对左室功能的影响

目的：选择原发性高血压病1—2级合并左心室肥厚的60例患者,分为补阳还五汤合温胆汤和开博通组30例,对照组开博通组30例,治疗6个月。运用超声心动图（UCG）、测血压和临床观察等手段,观察上述治疗对临床症状改善、血压下降、左室肥厚的逆转和左室舒张功能的疗效与作用。结果：中西药疗法能有效地使血压下降,总有效率93．33％,从而有效地预防和减轻靶器官的损害;能有效地减少室间隔及左室后壁厚度,使心室腔径缩小,左室重量指数下降;随着左室肥厚的逆转,左室舒张功能明显改善,SV与CO显著增加且与LVMI的下降呈正相关;对临床症状的改善明显优于对照组。可见,通过中西药结合辨证治疗能改善与高血压病有关的各种血液动力学和神经体液调节机制,达到降压、逆转左室肥厚、改善左室功能的作用。