不同栓塞范围的急性肺栓塞动物模型建立

目的：制备不同栓塞范围的急性肺栓塞动物模型,研究血流动力学变化与肺栓塞范围的相关性。方法:经导管注入犬自体血栓选择性栓塞肺动脉，通过控制注入血栓数量、速度，分别建立不同栓塞范围的急性肺栓塞动物模型；比较栓前、栓后15 min、30 min、1 h及2 h血流动力学指标变化，同时观察心脏超声影像学变化。结果:自体血栓均按要求阻塞相应肺动脉，肺栓塞形成后心输出量下降，肺动脉压力及肺毛细血管楔压显著增高，并在0.5 -1 h达到峰值，各血流动力学指标随肺栓塞范围增大而变化更显著。结论:此急性肺栓塞动物模型制作方法确切可行。     

频谱多谱勒技术评价冠心病人心室舒张功能

目的：采用频谱多谱勒技术观察冠心病人心室舒张功能改变。方法：冠状动脉造影确诊为冠心病患者61例，根据左室射血分数（EF）分为EF正常组（Ⅰ组，EF≥50％，33例），EF降低组（Ⅱ组，EF〈50％，28例）。正常对照组32例。频谱脉冲多普勒技术测量各组二尖瓣、三尖瓣血流频谱及肺静脉血流频谱参数；心导管测量冠心病组左室舒张末压（LVEDP）。结果：冠心病Ⅰ组左、右室舒张功能均可出现障碍，多呈松弛功能异常；冠心病Ⅱ组左室舒张功能障碍，多呈假性正常化；PVad-Ad与LVEDP呈正相关（r=0．72，P〈0．01）；以PVad-Ad〉0ms为标准来鉴别二尖瓣频谱假性正常化，敏感性为92％，特异性为80％；左右室舒张功能相关性分析（E／A：r=0．46，DT：r=0．54，P〈0．01）。结论：冠心病早期收缩功能正常时，左、右室舒张功能均可出现障碍；左室收缩功能异常时，左室舒张功能进一步减退，多呈假性正常化；PVad-Ad能准确地鉴别二尖瓣血流频谱假性正常化；冠心病人左右室舒张功能有较显著的相关性。     

左室部分切除可提高扩张性心肌病左室收缩末的回弹性

目的　用左室收缩末和主动脉回弹性及心室与主动脉连接评价左室部分切除术 (PL V )的效果。对象　 PL V前和 PL V两周后扩张性心肌病患者 11例 ,对照组 11例。方法　减容前后 ,右室起搏时 ,单投照位左室造影 ,同时测量股动脉压力。结果　 PL V使左室收缩末回弹性从 0 .5 2± 0 .2 7增加至 0 .19± 0 .0 8k Pa/ ml(P =0 .0 0 0 4) ,在左室质量变化 (P=0 .0 0 4)和收缩末容量改变 (P=0 .0 48)纠正后 ,左室收缩末回弹性维持有显著改变。PL V对主动脉搏回弹性没有影响 ,心室与主动脉连接从 3.2 5± 2 .17改善至 1.0 1± 0 .93(P=0 .0 17…     

急性肺栓塞家兔血流动力学参数及组织病理学改变

目的:观察急性肺栓塞(APE)家兔血流动力学及组织病理学变化。方法:从家兔颈静脉注入自体血栓,观察APE后家兔基本表现和死亡率,以及呼吸频率(RR)、平均呼吸深度(MDR);动态监测右心室压力(RVP)和最大上升(下降)速率±dp/dtmax以及颈动脉血压(AP)等血流动力学指标的改变,并行肺组织病理学检查。结果:APE家兔成活率为86.9%。注栓后RR和MDR持续升高,与栓塞前比较均具有统计学差异(P<0.05或P<0.01)。右心室收缩压(RVSP)栓塞即刻达峰值,6h下降到栓塞前,右心室舒张压(RVDP)与栓塞前比较无统计学差异。+dp/dtmax栓塞即刻达峰值,4h下降到栓塞前,-dp/dtmax栓塞即刻升高后恢复到栓塞前。APE后动脉收缩压(SAP)、舒张压(DAP)均持续下降,观察8h也未出现恢复。HE染色可见肺动脉内有血栓及肺小静脉扩张和大量炎性细胞浸润等病理改变。结论:自体血栓经颈静脉注入造成的APE可致血流动力学和肺组织形态学改变,尤以右心室收缩压和AP变化显著。     

基质金属蛋白酶及其组织型抑制剂活性及表达失衡与高血压性左心室重塑的关系

目的： 探讨慢性压力负荷增高时，大鼠左心室（LV）基质金属蛋白酶（MMPs）/组织型基质金属蛋白酶抑制剂（TIMPs）失衡与LV重塑的关系。方法：40只6周龄雄性卒中易感性自发性高血压大鼠（SHR-SPs）作为研究对象，10只同周龄雄性Wistar-Kyoto（WKY）大鼠作为对照。6个月后，以Millar压力容积导管评价2组大鼠的在体LV血流动力学，并对2组大鼠的心脏进行组织病理学、明胶酶谱和免疫印迹法分析。结果：反映LV收缩与舒张功能的血流动力学参数在2组间有显著差异（P＜0.05）；SHR-SPs心脏胶原容积分数、血管周胶原面积/管腔面积、心肌横断面积、心室壁动脉中膜面积/管腔面积均增高（P＜0.05）；心肌MMP-2活性、蛋白含量及TIMP-1蛋白含量在SHR-SPs中明显增高（P＜0.05）。结论：慢性压力超负荷能够导致心脏细胞外基质代谢失调及MMPs/TIMPs系统失衡，继而产生心室腔扩张、LV收缩与舒张功能障碍。     

心肺相互作用的研究进展

机械通气条件下的心肺相互作用均表现为胸内压(ITP)和肺容量二者的变化对血流动力学的影响,它们通过对左右心室前后负荷及静脉回流的影响产生不同的效应。心脏外组织亦对心脏充盈产生明显的影响。文章还分别论述了在COPD、急性左心功能衰竭、阻塞性睡眠呼吸暂停、ARDS及脱机过程中机械通气条件对血流动力学的影响。     

家兔急性肺栓塞对肺血管内皮细胞超微结构及血清一氧化氮含量的影响

目的 探讨急性肺栓塞（APE）对肺血管内皮细胞（PVECs）的结构及血清一氧化氮（NO）含量的影响。 方法 19只日本大耳兔,随机分成假手术组、栓塞2 h、4 h组(n=3)和8 h组（n=10）。通过输入自体血栓建立家兔急性肺栓塞模型后,采用HE染色光学显微镜下观察肺的病理组织学变化;透射电子显微镜下观察PVECs在肺栓塞2 h、4 h及8 h的超微结构变化;硝酸还原酶法测定相应时间点血清NO含 结果 HE染色显示栓塞组肺动脉内有血栓,肺间质炎性病变,肺淤血;透射电子显微镜显示,栓塞组PVECs水肿、破裂,线粒体肿胀,内质网空泡化,并随栓塞时间延长PVECs出现坏死脱落,细胞器溶解。肺栓塞2 h、4 h和8 h血清NO含量均低于栓塞前,与栓塞前比较差异有显著性意义（P＜0.05）。 结论 家兔APE可致PVECs超微结构改变和血清NO含量下降,且两者间关系密切。     

参麦注射液改善急性心肌梗死大鼠心功能与左室重构的机制初探

目的：观察了参脉注射液对心肌梗死后心功能和心室重构的影响，及其对心肌细胞凋亡的影响。方法：（1）结扎大鼠左冠状动脉前降支建立大鼠心肌梗死心室重构模型，随机分为心肌梗死后1、2周模型组，②参麦注射液治疗1、2周治疗组，另设两假手术组。多导生理记录仪测量：左室收缩压（LVSP）、左室舒张末压（LVEDP）、左室内压最大上升速率（＋dp／dtmax）和下降速率（-dp／dtmax）以反映左室收缩与舒张功能。测定心脏心脏总重量、左室截面直径，并计算心室重量指数；HE染色、Masson染色、透射电镜观察心结构改变。（2）乳鼠心肌细胞原代培养，AngⅡ诱导凋亡模型。利用荧光染色观察凋亡形态变化；流式细胞仪检测细胞凋亡、心肌细胞线粒体膜电位；激光共聚焦显微镜检测钙离子荧光强度。免疫组化染色检测Bcl-2／Bax、Caspase-3蛋白的表达。     

改变在体犬右心负荷对其电生理参数的影响

目的：搪塞改变在体犬右心负荷对其电生理参数的影响。方法：改变右房、右室负荷，测定右房，右室舒张期阈值（ＡＤＰ、ＶＤＴ）；右房、右室相对流尖期（ＡＲＲＰ，ＶＲＲＰ）和右房，右室有效不庆期（ＡＥＲＰ，ＶＥＲＰ）。结果：分级（Ａ级和Ｂ级），机械性地部分阻断右房至右室的血流，右房峰值压力（ＰＲＡＰ）升高和有右室峰值压力（ＰＲＶＰ）降低使人ＡＥＲＰ和ＶＲＲＰ延长；但未发现ＡＤＴ，ＶＤＴ有明显变化。亦未出现     

大鼠急性肺栓塞后SMP-30表达下降及其对细胞凋亡的影响

目的：研究大鼠急性肺栓塞模型肺组织中衰老标记蛋白质30(SMP-30)的表达变化及其对Fas诱导的细胞凋亡的影响。方法:建立大鼠急性肺栓塞模型，分别在急性肺栓塞后1、8、24和48 h进行支气管肺泡灌洗，然后开胸取出肺组织。常规提取肺组织的总RNA和总蛋白，以正常组为对照，采取半定量RT-PCR的方法研究SMP-30在mRNA水平表达的变化；采用Western blotting方法进一步验证SMP-30在蛋白水平表达的变化；采用免疫组织化学方法检测大鼠肺组织中SMP-30以及肺泡巨噬细胞中IL-8在肺栓塞前后表达的变化及其组织分布情况；采用TUNEL法研究急性肺栓塞后组织细胞的凋亡情况；最后采用ELISA法检测急性肺栓塞后肺泡灌洗液中sFasL的浓度变化。结果:在大鼠急性肺栓塞后的不同时点，SMP-30的mRNA水平和蛋白水平均逐渐降低，在24和48 h下降最为明显。免疫组化研究表明SMP-30主要分布在支气管黏膜上皮细胞和肺泡上皮细胞，急性肺栓塞后SMP-30在上述细胞内的表达均明显降低。TUNEL染色发现随着SMP-30表达的降低，肺组织内出现明显的细胞凋亡现象，同时肺泡灌洗液中sFasL的浓度升高，肺泡巨噬细胞内IL-8的表达也明显升高。结论:大鼠急性肺栓塞后肺组织内SMP-30的表达明显降低，可能促进Fas－FasL细胞凋亡系统的活化。     

应用CT评价急性肺栓塞对家兔心功能的影响*

 [摘要] 目的:建立家兔急性肺栓塞（APE）模型,应用64排心电门控CT评价APE对心脏功能及结构的影响并探讨其机制。方法: 7只健康日本大耳白兔通过自体血栓注入法复制APE模型,分别于APE前及APE后2 h、4 h、8 h行64排双源心电门控CT肺动脉造影（CTPA）,通过CT图像重建,应用Volume 及View软件计算出APE前后左心室和右心室收缩末期容积（LVESV和 RVESV）、舒张末期容积（LVEDV和 RVEDV）、收缩末期内径（LVESD和 RVESD）及舒张末期内径（LVEDD和 RVEDD）,CT图像寻找肺动脉血栓并与解剖观察对比分析。结果: APE后2 h、4 h及8 h各时点RVEDV、RVESV、RVEDD及RVESD明显增加（P<0.01）,LVEDV及LVEDD明显减少（P<0.05）,左、右心室每搏输出量（LVSV 和RVSV）减少（P<0.05）。64排CT肺动脉成像显示较大的肺动脉血栓表现为偏心充盈缺损,而较小的动脉血栓为肺动脉分支缺损;与解剖比较,发现较大动脉血栓的准确率达100%。结论: 家兔APE后右心室明显扩大,左、右心功能均受损,2 h后维持相对稳定。64排双源心电门控CT扫描对于判断APE后心功能障碍具有重要价值。     

Heart-rate-proportional oxygen consumption for constant cardiac work in dog heart

We studied whether there is an optimal heart rate (HR) that would minimize myocardial oxygen consumption (MVO2) per min for a constant minute cardiac work. We measured minute MVO2 (ml O2/min) of the left ventricle paced at increasing rates (100-200 beats/min) in 10 right-heart-bypassed dogs. In each experiment, cardiac output was kept constant with a constant-flow bypass pump, and mean aortic pressure was also kept constant by inflation or deflation of an intra-aortic balloon. Minute cardiac work was thus kept constant. Minute MVO2 was obtained as the product of mean coronary arteriovenous O2 difference and mean coronary blood flow drained from the collapsed right ventricle. Both left ventricular Emax (contractility index defined as the slope of the left ventricular end-systolic pressure-volume relation) and PVA (pressure-volume area as a measure of total mechanical energy of contraction) were obtained by an abrupt aortic occlusion method. The obtained-minute MVO2-HR relationship showed a good linear positive correlation (r = 0.824-0.995) in every heart. We accounted for this relationship by the changes in PVA and Emax that we had proposed as primary determinants of MVO2. We conclude that minute MVO2 for a constant minute cardiac work increased monotonically with increases in HR from 100 to 200 beats/min, being minimum at the lowest HR, and that this relation was ascribable to the HR-proportional increase in the MVO2 component for the excitation-contraction coupling.     

Left ventricle load impedance control by apical VAD can help heart recovery and patient perfusion: a numerical study

The aim of this work is to investigate the dependence between left ventricular load impedance control by an apical ventricular assist device (VAD) and the consequent benefits for pathological heart recovery. A pathological left ventricle with 34% contractility has been simulated in the assisted and nonassisted conditions. By means of an extended Kalman filter, left ventricular pressure-volume loops have been partially estimated and ventricular as well as circulatory quantities inferred. The heart operation mode, based on cardiac energetic criteria, is imposed by controlling the VAD filling phase. In the assisted condition, results show that the left ventricle end-diastolic volume, left atrial pressure, and wall stress all decrease; stroke volume, ejection fraction, ventricular efficiency, aortic pressure, and cardiac output all increase. Benefits are also evident for the right ventricle and systemic and pulmonary circulation. The strategy outlined in this work also shows that good results for heart recovery are achievable and a possible way to improve the functional properties of commercial pulsatile VADs.     

Anabolic steroids alter the haemodynamic responses of the canine left ventricle

The effect of an anabolic steroid on canine left ventricular function was studied by catheterization exposing control (n = 7) and methandienone-treated (n = 6) dogs to pacing, volume and isoproterenol tests at the beginning of the experiment and 6 weeks later. The physical performance of the animals was evaluated by submaximal exercise test (SMT), in which the steroid-treated dogs had lower heart rate than the sedentary controls (P less than 0.001). Heart weight was greater in the steroid than in the control group (P less than 0.05). Isoproterenol infusion increased the maximum value of the left ventricular pressure curve (dP/dtmax) less in the steroid-treated than in the control animals (P less than 0.05). Also heart rate was lower in the steroid than in the control group after inotropic load, while end-diastolic, end-systolic and stroke volumes decreased significantly more in the control group (P less than 0.05). Systemic vascular resistance decreased in the steroid treated animals, but remained unchanged in the control group (P less than 0.05 between the groups). During volume overload dP/dtmax increased in the control group but decreased slightly in the steroid group (P less than 0.05 between the groups). The pressure-volume diagram showed that the left ventricle of the steroid-treated animals worked on higher ventricular volumes than in the control group. In conclusion, long-term methandienone treatment results in cardiac hypertrophy in dogs, reduces its response to an inotropic loads and leads to working on larger ventricular volumes.     

缺氧性肺动脉高压大鼠右心室重构

摘要目的：研究缺氧性肺动脉高压大鼠右心室重构情况。方法：常压间断缺氧法复制缺氧性肺动脉高压大鼠模型，采用右心导管法测定平均肺动脉压力，通过测量右心室流入及流出道长度、左心室壁和右心室壁厚度、右心室和左心室 室间隔重量对其右心室重构情况进行定性研究。结果：缺氧14d后大鼠平均肺动脉压力显著升高，右心室流出道长度及右心室肥大指数显著增加，缺氧21d后右心室游离壁重量显著增加；右心室流人道长度及左、右心室壁厚度与对照组无统计学差异。结论：缺氧性肺动脉高压大鼠右心室早期表现为离心性肥大。     

Total internal mechanical work of ventricle assessed from quick release pressure-volume curve

A method is proposed for direct assessment of the total internal mechanical work of the cardiac ventricle from a pressure-volume diagram. First, a quick release pressure-volume curve of the lumped series elasticity of the ventricle is recorded. Next, this curve is transcribed on a pressure-volume loop diagram of a contraction of interest in such a way that the quick release curve passes through the end-systolic pressure-volume data point of the loop. Finally, planimetry of the triangular area bounded by the quick release curve, the isovolumic relaxation segment of the loop and the diastolic pressure-volume curve gives total ventricular mechanical internal work performed on the lumped series elasticity of the ventricle during systole. This method is much simpler and more direct than the conventional analytical method which requires a relatively simple geometric model of the ventricle, a formula for series elasticity with appropriate stiffness constants and a series of mathematical calculations based on many unverified assumptions on the shape, structure and mechanical properties of the ventricle.     

自制可调节肺动脉环缩装置对右心室作用实验研究

目的通过对动物右心室作用实验的研究,验证自制可调节肺动脉环缩装置的有效性。方法 12只健康雄性小尾寒羊,5～6个月龄,体质量26～37kg。随机分为实验组和对照组,每组各6只,体质量分别为（29.00±2.78）kg和（28.36±4.24）kg,差异无统计学意义（P=0.722）,从左侧第二肋间进胸,游离肺动脉主干,置入自制可调节肺动脉环缩装置,向球囊内注入0.9%NaCl溶液,逐渐增加右心室压力,进行心室训练,达到训练标准所需时间为9～18d。观察超声下右心室形态、血流动力学及心肌组织病理学变化。结果超声下右心室形态、室间隔位置、游离壁厚度均较训练前发生明显改变;血流动力学结果表明右心室/左心室收缩压力比值大于0.6,达到临床上心室训练的标准;右心室的收缩功能（P〈0.05）和舒张功能（P〈0.001）均得到了增强;病理检查结果右心室游离壁厚度及质量、右心室肥大指数、心肌细胞横径与对照组比较差异存在显著统计学意义（P〈0.001）。结论该装置能够达到肺动脉环缩、训练心室的目的 ,并且可双向调节,使用方便,效果可靠。     

Immunohistochemical evaluation of cardiac connexin43 in rats exposed to low-frequency noise

Introduction: Low-frequency noise (LFN) leads to an abnormal proliferation of collagen and development of tissue fibrosis. It has been shown that myocardial fibrosis in association with gap junction remodeling occurs in several cardiac diseases and can be implicated in the development of ventricular tachyarrhythmias. We previously reported a strong development of myocardial fibrosis induced by LFN in rats but it is not known whether LFN induces any modification on cardiac connexin43 (Cx43). Objectives: The aim of this study was to evaluate modifications on cardiac Cx43 induced by LFN in Wistar rats. Methods: Two groups of rats were considered: A LFN-exposed group with 10 rats submitted continuously to LFN during 3 months and a control group with 8 rats. The hearts were sectioned from the ventricular apex to the atria and the mid-ventricular fragment was selected. The immunohistochemical evaluation of Cx43 was performed using the polyclonal antibody connexin-43m diluted 1:1000 overnight at 4°C. Quantifications of Cx43 and muscle were performed with the image J software and the ratio Cx43/muscle was analyzed in the left ventricle, interventricular septum and right ventricle. Results: The ratio Cx43/muscle was significantly reduced in LFN-exposed rats (p=0.001). The mean value decreased 46.2%, 22.2% and 55.6% respectively in the left ventricle (p=0.008), interventricular septum (p=0.301) and right ventricle (p=0.004). Conclusions: LFN induces modifications on cardiac Cx43 in rats. The Cx43 reduction observed in our study suggests that LFN may induce an arrhythmogenic substrate and opens a new investigational area concerning the effects of LFN on the heart.     

Asymptomatic Continuous Murmur Due to Acquired Coronary Artery to Right Ventricular Fistula

An unusual case of an acquired coronary artery to right ventricular fistula is reported. A new continuous murmur was noted one month following a puncture wound to the precordium. Cardiac catheterization documented a left anterior descending coronary artery to right ventricular communication with a small left to right shunt and normal cardiac pressures. The angiographic appearance was that of a false aneurysm of the anterior descending artery with rupture into the right ventricle. The patient has been followed for 36 months and is asymptomatic with no evidence of myocardial ischemia or infarction. Because of the small size of the fistula and its intracardiac position, conservative treatment has been employed.     

Dynamics of the interventricular septum and free ventricular walls during selective left ventricular volume loading in dogs

A previous study suggested that a change in the position of the interventricular septum played an important role in regulating cardiac performance during selective right ventricular volume loading. In the present study the cardiac response to selective left ventricular volume loading induced by a shunt between the subclavian artery and the left atrium was examined in anesthetized open-chest dogs. Opening the shunt increased left and reduced right ventricular stroke volume, particularly after blood volume expansion. The end-diastolic transseptal pressure difference increased. Myocardial segment length in the septum and free walls of both ventricles and the distances between the septum and the free walls were measured by an ultrasonic technique. Comparisons at similar left ventricular stroke volume with the shunt open and closed showed that the Frank-Starling mechanisms of the free wall of the left ventricle and the septum were stimulated less with the shunt open. At similar right ventricular stroke volume the end-diastolic dimension of the right ventricular free wall was larger with the shunt open. The distance decreased across the right ventricle and increased across the left ventricle when the shunt was open. We conclude that a change in the position of the septum improves left and reduces right ventricular performance during selective left ventricular volume loading.