外源性促红细胞生成素对压力超负荷引起的小鼠左心功能障碍的保护作用

目的探讨外源性促红细胞生成素对压力超负荷引起小鼠左心功能障碍的保护作用。方法选取45只C57BL/6J雄性小鼠,主动脉弓缩窄术(TAC)后,将小鼠随机分为假手术组(Sham)、模型组(TAC-PBS)和治疗组(TAC-EPO),每组15只。采用M型超声心动图分别测量小鼠术前和术后2、4、6、8周左室舒张末期直径、左室收缩末期直径、左室短轴缩短率、舒张末期室间隔厚度、左室游离壁厚度和心室率;术后8周进行心导管测定,测量左心室收缩峰压、左室舒张末压和心室率。结果超声心动图示,与假手术组比较,模型组和治疗组小鼠左心室舒张和收缩末期直径均增加(P0.05),左心室短轴缩短率均减少(P0.05);但经EPO治疗后,与模型组相比,治疗组小鼠左心室舒张和收缩末期直径显著降低(P0.05),左心室短轴缩短率显著增加(P0.05)。结论外源性促红细胞生成素对压力超负荷引起的小鼠左心功能障碍的保护作用可能通过降低左心室扩张而实现。     

原发性高血压病视网膜中央动脉血流与左心室功能关系的多普勒观察

目的：研究原发性高血压病（PH）视网膜血管与左心室功能的相关性。方法：采用多普勒技术对比检测了52例PH和50例健康自愿者的机网膜中央动脉（ACR）血流及左心室功能。结果：病例组左心室舒张功能指标（除舒张早期血流峰值流速外）与对照组差异非常显著（P＜0．01），收缩功能指标与对照组无差异（P＞0．05）。病例组ACR舒张期、收缩期及其平均血流速率均与对照组差异非常显著（P＜0．01）。结论：PH左心室舒张功能按收缩功能变化更明显，在收缩功能尚未改变之前，ACR血流已有异常变化。     

基于微机的心脏动力学参数的检测

本文在左心室舒缩周期中，应用微电脑技术，将模拟ＥＣＧ、ＬＶＰ、主动脉血压及血流信号经１２位Ａ／Ｄ转换器转变成数字量，自动分析计算出有关的心肌收缩及舒张功能。系统利用Ｒ波顶点来确定等容收缩期的起始点，用ＬＶＰ导数最大值作为等容收缩期终点，从ＬＶＰ导数最大值开始到导数波出现负急剧下降的起始点作为左室射血结束时，系统有实时处理和事后处理两种工作模式，并将四道 原始信号长时间地不间断地，录在计算机硬盘上，     

人工心脏泵辅助对左心室血流动力学影响的数值研究

目的采用数值模拟方法研究人工心脏辅助装置植入对左心室内血流动力学的影响。方法首先利用心血管集中参数模型获取了健康状态、心衰状态以及人工心脏泵辅助状态下收缩末期左心室三维几何模型,其中选取超弹性材料Ogden为心肌材料,以左心房压力,主动脉压力以及通过左心室容积计算获取的左心室壁面位移作为边界条件,利用CFD方法对上述三种情况进行左心室的数值模拟。同时对比了健康时的模拟结果和生理状态下的左心室压力,以及心衰和人工心脏泵辅助两种状态下的血流动力学指标的差别。通过左心室压力和流速等评价灌注和负荷的情况,通过壁面切应力和涡流,评价人工心脏泵辅助后的左心室血流动力学变化规律。结果健康状态下模拟的左心室压力与生理指标相符合。在心衰和人工心脏泵辅助状态下,收缩期内左心室压力与健康状态比分别降低了1718 Pa和8455 Pa,辅助后左心室最大压力下降速度高于心衰时。人工心脏泵辅助后,舒张期壁面切应力峰值由4.3 Pa降低至3.8 Pa,收缩期壁面切应力峰值由4.1 Pa降低至1.3 Pa,射血速度峰值由1.61 m/s降低至0.68 m/s,主动脉瓣开放时间由0.25 s增加至0.65 s,左室射血分数由43.6%增加至52.7%,心室底端漩涡持续时间由0.35 s增加至0.51 s,顶端漩涡出现血流分离。结论左心室压力对比表明本研究方法可以用来模拟左心室的行为。人工心脏泵辅助能够快速降低心室内压力和心室负荷,增加灌注时间,提高器官灌注,降低左心室壁面切应力以及提高左心室内血液流场的涡流强度,延长涡流持续时间。     

犬离体心肌应力-应变关系超声印压方法研究

目的：探讨超声循环印压检测心肌被动力学属性可行性，为活体检测提供基础。方法：通过循环印压犬离体心室肌，获得印压力和心肌形变实验数据。结果：以准线性粘弹性理论（QLV）模型处理所获得的应力、应变数据，获取左心室心尖和游离壁心肌被动力学属性参数A、B、C、D、E，两者的参数比较无差异（P〉0.05）。结论：介入超声循环印压检测心肌被动力学属性是可行的。可望在话体检测不同状态下舒张期心肌被动力学属性，进一步从力学机制层面深入认识舒张性心力衰竭。     

双源螺旋CT对非缺血性二尖瓣反流机制的研究

目的运用双源螺旋CT（DSCT）探寻非缺血性二尖瓣反流的反流机制。方法超声诊断为二尖瓣反流并行CT俭查的46例患者．其中男性28例,女性18例;年龄37～81岁,平均年龄63．57岁。二尖瓣反流组依据多普勒超声检查分为轻度反流组（20例）、中度反流组（14例）、重度反流组（12例）。分别在cT图像上测量收缩中期幕状面积、幕状高度、二尖瓣瓣环前后径、联合间距离等二尖瓣装置形态参数。另随机选择无二尖瓣反流的体检者43例作为止常埘照组．．结果小同程度二尖瓣反流组在幕状面积、幕状高度、瓣环前后径、收缩中期和舒张末期瓣环面积较正常对照组差异有统计学意义（P〈O．05）。而瓣环联合间径差异无统计学意义（P〉0．05）。不同程度二尖瓣反流组在舒张期左心室短轴长度、球形度．收缩期左心室长径、舒张末期容积（EDV）、收缩末期容积（ESV）差异有统计学意义（P〈0．05）,、乳头肌间距变化度、左心事长径位移度组间差异均无统计学意义（P〉0．05）。结论DSCT功能检查对二尖瓣反流机制研究有重要价值,、非缺血性二尖瓣反流乃因心室-瓣膜环受过重前负荷而扩张．导致前外侧乳头肌腱索对前叶体部的过度牵拉．致使精确闭合的双侧瓣叶产毕前叶的云云h不对称导计对合而稠的减少,产生反流。     

IABP在临床的应用和护理

主动脉内球囊反搏(IABP)：(Intra-aortic bal oon pump)是机械性辅助循环方法之一,是由固定在导管的圆柱形气囊构成,将其安放在胸主动脉部位,通过物理作用,提高主动脉内舒张压,增加冠状动脉供血和改善心肌功能。主动脉内球囊反搏的工作原理：导管近端位于左锁骨下动脉末梢,远端位于肾动脉。主动脉内球囊反搏泵工作时驱动气体往返进出气囊。在心脏搏动的舒张期,球囊从排气状态突然膨胀充气,在胸降主动脉内占有了一定的体积,将原来占据该体积的血液顺、逆着动脉走行向终末端器官灌注。在收缩期,球囊从充气状态突然收缩排气,其所占据的体积被周围血液迅速回流填充。其产生双重血流动力学变化：主动脉收缩压降低,主动脉舒张压升高,平均动脉压升高,左心室舒张末期压力降低,左心室后负荷降低,射血分数增加,心输出量增加,心内膜下心肌存活率增加,体循环血管阻力下降。     

无创监测表阿霉素心脏毒性-组织多普勒超声心动图

目的： 利用组织多普勒和常规超声心动图评估淋巴瘤患者表阿霉素心脏毒性。 方法： 20例接受表阿霉素化疗的淋巴瘤患者，表阿霉素总累计量(450±75)mg/m2，每个疗程治疗前进行组织多普勒和常规超声心动图检查。健康对照组20例。常规超声心动图指标包括左室舒张末内径（LVEDD），左室收缩末内径（LVESD），左室射血分数（LVEF），二尖瓣口血流速度（早期速度E,晚期速度A及两者比值E/A）；组织多普勒指标有二尖瓣环左室侧壁处组织多普勒峰值速度（收缩峰速S，舒张早期峰速E，舒张晚期峰速A及E/A）。 结果： 与治疗前相比，常规超声心动图收缩期指标LVEDD、LVESD、LVEF在累计量达到450 mg/m2才出现显著差别［LVEDD (55.4±10.2)mm vs (42.2±8.1)mm；LVESD (34.2±7.9)mm vs (24.5±5.3)mm；LVEF (58.1±6.5)% vs (68.2±7.4)%,P<0.05］，常规超声心动图舒张期指标E/A在累计量达到375 mg/m2才出现显著差别［(0.88±0.16) vs (1.22±0.21)，P<0.05］；而组织多普勒收缩期指标S在累计量达到300 mg/m2就出现显著差别［(8.1±2.5)cm/s vs (10.2±3.6)cm/s，P<0.05］，组织多普勒舒张期指标E/A在累计量达到225 mg/m2即出现统计学意义的差别［(0.90±0.18) vs (1.13±0.23)，P<0.05］。与健康对照组相比，20例淋巴瘤患者第一次治疗前各指标无明显差别（P>0.05）。 结论： 在监测表阿霉素心脏毒性上，组织多普勒超声心动图较常规超声心动图能较早期和较敏感发现变化，且舒张功能变化早于收缩功能变化。     

定量组织速度成像对阻塞性睡眠呼吸暂停综合征患者腭咽成形术前左心功能的研究

目的应用定量组织速度成像(QTVI)技术,对拟行改良腭咽成形术的阻塞性睡眠呼吸暂停综合征(OSAS)患者左心室功能的早期变化进行研究。方法 A组,35例OSAS患者,均为男性,年龄21～58岁,平均年龄41.27岁。B组33例,健康者,均为男性,年龄22～55岁,平均年龄39.57岁。B组年龄、性别、体质量指数与A组相匹配,为对照组。用常规超声心动图和QTVI新技术,对其心脏形态结构和功能进行各节段参数测定。结果 A组与B组间常规超声参数比较:主动脉根部内径(AOD)、左心室舒张末期内径(LVDd)、左心室后壁厚度(LVPWT)和二尖瓣前向血流速度舒张早期与舒张晚期的比值(E/A)差异有统计学意义(P<0.05);二尖瓣环部分节段QTVI技术参数中舒张早期峰值速度(Ve)部分节段减低、舒张晚期峰值速度(Va)部分节段增高、Ve/Va比值部分节段减低,与B组比较差异有统计学意义(P<0.05),收缩期峰值速度(Vs)二组间差异无统计学意义(P>0.05)。结论 QTVI检测的二尖瓣环运动速度在判断左心室收缩和舒张功能早期变化方面有重要价值,能早期发现OSAS患者部分指标已有增加趋势,为临床手术前、后监测左心功能变化提供参考数据。     

三维斑点追踪技术评价心脏再同步化治疗患者左心室心肌力学初步改变

目的应用三维斑点追踪技术(3D-STI)评价左心室心肌力学变化,探讨3D-STI在评价心脏再同步化治疗(CRT)患者左心室收缩功能中的应用价值。方法选择接受CRT且成功植入三腔起搏器的心力衰竭患者20例,其中男性14例,女性6例;年龄18~69岁,平均年龄47岁。于起搏器植入术前及术后6个月进行常规超声测量左心室舒张末期容积(LVEDV)、左心室收缩末期容积(LVESV)和左心室射血分数(LVEF);应用3D-STI测量左心室整体3D应变(D3S)、纵向应变(LS)、环向应变(CS)、径向应变(RS);左心室整体旋转角度峰值(LVrot)和左心室整体扭转角度峰值(LVtw)、左心室整体最大径向位移(Dr)、纵向位移(Dl)、三维位移(D3d)等指标。比较术前和术后上述指标之间的差异,并将以上指标进行相关性分析。结果 CRT术后D3S、LS、CS、RS较术前显著提高,LVrot、LVtw、Dr、Dl和D3d均较术前明显增加,差异均有统计学意义(P0.05)。相关分析显示D3S、LS、CS、RS、LVrot、Dr、Dl和D3d与LVEF均相关(r=-0.63、-0.56、-0.51、0.60、0.38、0.80、0.49及0.45,P0.01),LVtw与D3S、LS、CS、RS、Dr、D3d间均有良好相关性(r=-0.45、-0.35、-0.39、0.37、0.37、0.45,P0.01)。结论 3D-STI能有效观察左心室心肌力学改变,准确评价左心室收缩功能,对评价CRT术后疗效有重要意义。     

Left ventricular pressure transmission to myocardial lymph vessels is different during systole and diastole

In six open-thorax-anaesthetized dogs with paced hearts and a retrogradely cannulated epicardial lymph vessel, the sensitivity of myocardial lymph pressure to left ventricular pressure during systole and during diastole was determined. The lymph vessels were cannulated using PE-90 tubing, and lymph pressure was measured by connecting the cannula to a microtip pressure transducer. To obtain the systolic sensitivity, left ventricular pressure was changed by clamping the descending aorta, which caused left ventricular pressure to increase. The diastolic sensitivity was obtained from natural variation to left ventricular pressure caused by atrial contractions during induced long diastoles. The mean ratio of the pulse in lymph pressure to the pulse in left ventricular pressure was determined: systole: 0.069±0.013, n=213, diastole: 0.76±0.16, n=249 and, if possible, linear regression analysis between lymph and left ventricular pressure was performed. The systolic regression coefficients could be determined in six dogs and the diastolic coefficients in three dogs. During long diastoles lymph pressure variations are on average 76 per cent of those in the left ventricle. However, during systole, the sensitivity of lymph pressure to left ventricular pressure is more than ten times lower. It is not unlikely that the structural embedment of lymph vessels within the myocardium is such that volume variations by cardiac contraction are limited.     

主动脉瓣狭窄对左心室血流特性的影响

基于CT断层扫描数据,对心脏左心室进行三维重构和模型优化。结合心肌壁面的运动特性,建立左心室几何模型过流边界运动的数学模型。通过水力半径表征主动脉瓣的狭窄程度,采用动网格技术研究主动脉瓣狭窄对左心室血液流动的影响。研究发现不同程度主动脉瓣狭窄时,水力半径与主动脉瓣狭窄程度负相关,出口面积减小,收缩期出口处速度与压力升高,剪切应力增加。舒张期,速度与压力出现先增大后减小的规律。当水力半径较小时,左心室瓣膜处剪切应力较大,收缩初期剪切应力最大为0.81 Pa。通过动态模拟对心脏的仿真研究,为后续心脏的研究提供重要的参考价值。     

多普勒超声与同步心电图测定正常人左室收缩期时相的方法学研究

探讨以多普勒超声结合同步心电图定义左室收缩期时相的可行性。采用多普勒超声与同步心电图同时显示主动脉瓣口血流频谱及心电图的波形 ,测定 13例正常人左室收缩期各时相的时间与二维容积参数 ,比较常规法与多普勒超声法的测值之间差异 ;分析两种方法测值之间相关性和一致性。结果 :两种方法测量的左室收缩末期的时间无统计学差异 (P>0 .0 5 ) ,两者具有高度线性相关关系 (r=0 .91,P<0 .0 1)。 Bland- Altm an分析两种方法测值一致性良好 ;两种方法测量的左室收缩末期的容积无统计学差异 (P>0 .0 5 ) ,两者具有高度线性相关关系 (r=0 .97,P<0 .0 1)。两种方法测量的容积一致性良好 ;多普勒法测量的左室等容收缩末期的容积和常规法测量的左室舒张末期的容积经比较无统计学差异 (p>0 .0 5 ) ,两者具有高度线性相关关系 (r=0 .98,P<0 .0 1)。多普勒法测量左室等容收缩末期容积与常规法测量左室舒张末期容积一致性良好。多普勒超声结合同步心电图确定左室收缩期时相的方法是可行的 ,并与常规法具有相互替代性。     

Computer analysis of cardiovascular parameters

A computer program is described for the analysis of several cardiovascular parameters frequently measured or derived in the chronically instrumented dog model. Data are stored on magnetic tape and are subsequently analyzed with the Apple IIe microcomputer equipped with the ADALAB (Interactive Microware, Inc.) analog-to-digital convertor. Not limited to the chronically instrumented animal model, the program is capable of analyzing left ventricular pressure, three channels of regional myocardial segment length, coronary flow velocity as measured by the Doppler ultrasonic flow technique, and two channels of systemic arterial pressure. Derived data include: left ventricular dP/dtmax, left ventricular pressure-heart rate product, left ventricular ejection time, tension time index; percent segment length shortening and velocity of shortening, dL/dt(s)max, regional stroke work and power, duration of systole and diastole; mean coronary flow velocity, peak diastolic and systolic flow velocity, and true mean systemic arterial pressure.     

Quantitative evaluation of intra-aortic flow disturbance by the fluid momentum index: Effect of the left ventricular systolic function on the hemodynamics in the aorta.

The combined hemodynamics in the left ventricle and aorta were analyzed numerically to investigate how the hemodynamics in the aorta varies with changes in left ventricular systolic function quantified as the ejection fraction (EF). EFs of 0.3, 0.5, and 0.7 were defined by controlling the total volume ejected during systole, while maintaining the ventricular volume at the end of diastole. The results showed that although the variation in left ventricular systolic function resulted in a change in the magnitude of the flow velocity, the intraventricular and aortic flows, including the secondary flows at the aortic valve orifice, were essentially the same regardless of the EF. To evaluate the strength of the secondary flow relative to the axial flow, the flow momentum index, FMI, was proposed. Spatiotemporal maps of the FMI obtained with different EFs had similar topological patterns, suggesting that the left ventricular systolic function contributed less to the efficiency of conveying blood in the axial direction in the aorta. Systolic function had a minimal effect on the spatiotemporal distribution of the maximum wall shear stress (WSS). A comparison of the spatiotemporal maps of the FMI and WSS revealed that the spatiotemporal maximum of WSS that occur in peak systole did not correspond to that of the FMI, demonstrating that the spatiotemporal maximum WSS was not induced by the helical flow. These results demonstrated that the left ventricular systolic function is not reflected in the global hemodynamics in the aorta and addressed potential of the FMI as an index to quantify the aortic flow disturbances.     

Relation of mitral valve opening and closure to left atrial and ventricular pressures in the intact dog

The exact times of mitral valve opening and closure were determined in dogs under varying hemodynamic conditions in 143 cardiac cycles (five experiments). Radiopaque markers had been sutured to the cusps and the valve annulus 7-124 wk before the studies. Valve opening and closure times were correlated with simultaneously obtained high-fidelity intracardiac pressures. Closure of the mitral valve was completed 5-105 ms after the atrial-ventricular pressure crossover; the time interval between the onset of ventricular systole and the instance of complete valve closure varied less (10-40 ms). These observations suggest that in the intact heart alpha, rapid mitral cusp closure at the end of diastole is initiated and completed by ventricular systole alone, and beta, the ventricular isovolumic contraction period might be shorter than assumed. Opening of the valve during ventricular relaxation was characterized by 1) initial separation of the markers placed on the free edges of the cusps, of variable duration, apparently due to alterations in ventricular geometry, and 2) a rapid opening motion which clearly preceded the diastolic pressure crossover by 5-60 ms. This finding would suggest that ventricular isovolumic relaxation might be shorter than generally accepted, although the mechanism of early opening is not adequately explained by the data.     

Identification of canine coronary resistance and intramyocardial compliance on the basis of the waterfall model

This study was performed to elucidate the effects of cardiac contraction on coronary pressure-flow relations. On the basis of the waterfall mechanism, a lumped model of the coronary arterial system is presented consisting of a proximal (epicardial) compliance, a coronary resistance, and an intramyocardial compliance. A “back”-pressure, assumed to be proportional (constant k) to left ventricular pressure, impedes flow. From steady-state measurements of circumflex coronary artery flow and inflow pressure, together with left ventricular pressure, the values of the three model parameters and the constant k have been estimated. In the control condition proximal compliance is found to be 1.7×10⁻¹² m⁴s²kg⁻¹, intramyocardial compliance 110×10⁻¹²m⁴s²kg⁻¹, and resistance 7.5×10⁹kgm⁻⁴s⁻¹. The proportionality constant k is close to unity. Effects of changes in left ventricular pressure and inflow pressure and the effect of vasoactive drugs on the parameters are also investigated. Changes in coronary resistance are always opposite to changes in intramyocardial compliance. Sensitivity analysis showed that epicardial compliance plays its major role during isovolumic contraction and relaxation; resistance plays a role throughout the cardiac cycle but is more important in diastole than in systole, whereas intramyocardial compliance plays a role in systole and in early diastole.     

Instantaneous pressure-volume relationship of right atrium during isovolumic contraction in canine heart.

We studied the contraction of the right atrium in an excised cross-circulated heart preparation. Atrial volume and instantaneous atrial pressure were measured in a water-filled balloon fitted in the spontaneously contracting right atrium. The relation of instantaneous pressure to volume was analyzed by collecting pressure data from multiple isovolumic contractions with different volumes but measured at multiple identical time points in the contraction cycle. The relation was found to be quasi-linear during most of atrial systole and diastole. A linear regression formula P(t) = K(t)[V- VD(t)] was therefore fitted to the data. K(t) and VD(t) of the regression formula are the slope and the volume axis intercept in the pressure-volume plane, respectively. When the atrium beat spontaneously at a regular sinus rhythm with no inotropic intervention. K(t) increased during systole and decreased during diastole, whereas VD(t) decreased during systole and increased during diastole. The average value of K was 13 +/- 1.7 (SE) mmHg . kg . ml-1 at the end of diastole and 33 +/- 0.02 (SE) mmHg . kg . ml-1 at the end of systole. The average value of VD was 0.303 +/- 0.017 (SE) ml . kg-1 at the end of diastole and 0.212 +/- .025 (SE) ml . kg-1 at the end of systole. Enhancement of contractility with epinephrine or Ca2+ significantly increased the value of K at the end of systole, but it did not significantly affect either K at the end of diastole or VD at the end of systole and diastole.     

Sympathetic afferent nerve activity of right heart origin.

Six mongrel dogs anesthetized with sodium pentobarbital and paralyzed with gallamine triethiodide were studied on total cardiopulmonary bypass. This study verified the existence of right heart mechanoreceptors whose afferent nerves traverse the upper thoracic white rami communicantes. these mechanoreceptors were studied by observing changes in average maximum, and total nerve spike frequency when right atrial and right ventricular systolic and diastolic pressures were altered by means of intracardiac balloons. Receptors that responded to volume and pressure changes were found in both the right atrium and right ventricle. Nerve activity in these afferents increased with increasing right atrial and right ventricular pressures. These mechanoreceptors were more responsive in the upper physiological ranges of right heart pressures. In most nerve fibers studied, maximum activity occurred during both right atrial and right ventricular diastole.     

Application of finite-element analysis with optimisation to assess thein vivo non-linear myocardial material properties using echocardiographic imaging

An application of finite-element analysis with an optimisation technique to assess the myocardial material properties in diastasisin vivo is described. Using the data collected from an animal model, the three-dimensional geometry of the left ventricular chamber, at several times in diastole, was reconstructed. From the measurement of the ventricular chamber pressure during image acquisition, finite-element analysis was performed to predict the expansion during diastasis. Initially, by restricting the motion of the epicardial nodes and computing the reaction forces, an ‘equivalent pericardial pressure’ was determined and applied in subsequent analysis. The duration of diastasis was divided into three or four intervals and the analysis was performed at each interval to assess the material properties of the myocardium. Using such a step-wise linear approach, the non-linear material properties of the myocardium during passive expansion was determined. Our results demonstrated that the computed ‘equivalent pericardial pressure’ increased with and was smaller than the corresponding left ventricularchamber pressure. The passive myocardium exhibited a linear tangent modulus against chamber pressure relationship which is equivalent to an exponential stress/strain relationship, similar to those suggested byin vitro studies.