右心导管法测大鼠肺动脉压力的改良

目的:目前常用的测量大鼠肺动脉压力的右心导管法存在一定的缺陷,且很难得到典型的压力曲线图。本实验对大鼠经颈外静脉插管与测压的方法进行改良,同时与已有报道的实验结果进行比较,并提供正常SD大鼠右心房、右心室及肺动脉的压力参考值及典型的压力曲线图,以协助研究人员判断导管位置,及时调整导管的深度和方向,快速测出肺动脉压力。方法:雌雄不分的清洁级SD大鼠共30只,体重180~230 g,6~7周龄。应用自制的末端呈一弧形的PE-10管,采用改良后的右心导管法,经颈外静脉插入大鼠心腔及肺动脉,检测并计算大鼠右心房、右心室和肺动脉的收缩压、舒张压及肺动脉平均压。结果:右心房压力波动较平缓,呈小波浪形;右心室压力曲线波动大,骤升骤降;肺动脉压力曲线有重搏波。正常SD大鼠右心房舒张压为(2.03±2.56)mmHg,收缩压为(2.82±1.85)mmHg;右心室舒张压为(5.72±3.99)mmHg,收缩压为(18.73±4.80)mmHg;肺动脉舒张压为(15.27±2.64)mmHg,收缩压为(18.49±2.53)mmHg,肺动脉平均压为(16.34±2.32)mmHg。右心室收缩压与肺动脉收缩压无明显差异(P0.05)。结论:改良后的方法可准确到达大鼠肺动脉,提供的压力参考值及曲线图有助于研究人员顺利完成测压实验。     

大鼠经颈外静脉导丝引导插管测肺动脉压与传统方法的比较

目的探讨大鼠经颈外静脉插管方法及测肺动脉压的最佳方法。方法将80只雄性SD大鼠按随机分组原则分成2组：经导丝引导插管测肺动脉压组（G组）,传统方法插管测肺动脉压组（T组）,每组均40只。记录插管操作一次成功率、多次调整成功率（n≤4次）、总成功率、一次插管时间、总插管时间、及一次测压时间、总测压时间及肺动脉高压大鼠肺动脉压力数值。结果 G组比T组插管操作一次成功率、多次调整成功率（n≤4次）、总成功率更高（P〈0.05）,G组比T组的一次插管时间、总插管时间以及一次测压时间、总测压时间要短（P〈0.01）,G组所测的肺动脉高压大鼠的肺动脉压力比T组所测的高（P〈0.01）。结论经导丝引导插管测肺动脉压法插管和测压具有成功率高、准确到达肺动脉、数据更准确、操作省时的优点。与用传统方法插管测肺动脉压组相比较,是一种更好的对大鼠进行颈外静脉插管和测肺动脉压的方法。     

袋鼠式护理体位在缓解婴幼儿静脉穿刺疼痛中的应用

目的探讨袋鼠式护理体位在缓解婴幼儿静脉穿刺疼痛的干预效果。方法选取我院门诊接受静脉穿刺治疗的婴幼儿100例,采用自身对照法进行研究,单日注射为对照组,双日为实验组。对照组按操作常规进行静脉穿刺,实验组在静脉穿刺前20ming及静脉穿刺后5min实施袋鼠式环抱体位进行常规操作,观察两组婴幼儿疼痛表情出现时间、开始啼哭时间以及持续时间。结果实验组婴幼儿进行静脉穿刺时开始啼哭时间、疼痛表情出现时间均明显晚于对照组(P0.05),啼哭持续时间、疼痛表情持续时间均明显短于对照组(P0.05)。结论袋鼠式护理体位可有效缓解婴幼儿静脉穿刺疼痛,且该法操作简单,无不良反应。     

兔急性肺血栓栓塞模型建立及右心室压和心电图监测

目的建立操作简便,存活率高的急性肺动脉血栓栓塞（acute pulmonary thromboembolism,APTE）模型并监测右心室压及心电图,为研究肺栓塞（pulmonary embolism,PE）的病理生理及临床诊断治疗提供实验基础。方法兔麻醉后,经右侧颈总静脉插管至右心室观察正常右心室压。然后经此导管注入4个直径2 mm、长5 mm的长柱状自体血栓栓子建立兔急性PE模型。10只PE兔监测右心室压及心电图至栓塞后80 min。过量麻醉处死动物,取肺脏固定做病理检查。结果右心室导管的插管成功率92.45%,平均右心室正常压力（32.69±8.32）mmHg。PE模型的栓塞率100%,存活率87.76%。模型建立后右心室压平均增高（6.75±6.82）mmHg,51.35%出现异常心电图波形。结论1.兔正常右心室压为（32.69±8.32）mmHg。2.自体血栓栓子经颈静脉入口右心室注入法建立兔急性PE模型存活率高,右心室压可作为判断急性PE模型成功建立的指标。3.仅部分PE出现心电图异常,心电图异常不能作为判断兔PE的指标。     

野百合碱性肺动脉高压大鼠右心功能分析

目的研究肺动脉压力演变和右心室功能演变之间的关系。方法将MCT诱导的4组肺动脉高压(pulmonary artery hypertension,PAH)模型组(每小组12只),分别在第1、2、3、4周应用右心导管测量肺动脉压力,MRI右心功能动态检测,观察肺动脉压力和MRI参数演变关系。比较对照组、PAH模型组各组间的相关各参数差异。采用SPSS 17.0统计软件,应用Pearson相关性分析,评价右心室射血分数,右室舒张末期容积,右室收缩末期容积分别与平均肺动脉压的相关性,组间比较采用完全随机分组的t检验,P0.05为差异有显著性。结果注射野百合碱后1~4周,48只模型组大鼠的右心室射血分数、右心室舒张及收缩末期容积与平均肺动脉压有很好的相关性(分别为r_(RVEF)=-0.823,r_(RVEDV)=0.732,r_(RVESV)=0.803)。注射野百合碱前两周,野百合碱组大鼠的平均肺动脉压、右心室射血分数、右室舒张末期和收缩末期容积与对照组比较差异无显著性(P0.05)。3~4周后,以上各参数与对照组比较差异有显著性(P0.05)。结论随着大鼠的肺动脉压增高,右心室射血分数逐渐降低,右心室舒张末期及收缩末期容积逐渐增加。对于大鼠慢性肺动脉高压模型的监测,MRI可以准确快速测量各项参数变化,右心室舒张末及收缩末期容积、射血分数等参数是提示肺动脉高压的敏感参数。     

激光心肌血管重建缓解心绞痛的机制研究

目的:探讨激光心肌血管重建(TMLR)缓解心绞痛的机制。方法:犬冠状动脉前降支结扎加空气栓塞造成心肌梗塞模型,随机分为实验组(n=6)和对照组(n=6)。术后4周实验组心肌梗塞区行TMLR,对照组做假手术。第一次术后8周多巴酚丁胺试验前、后心大静脉内抽取血样,放射免疫法测定血浆腺苷含量,RT-PCR检测心肌腺苷A1受体mRNA的表达变化,比较其积分光密度值。结果:在静息状态,实验组冠状静脉内血浆腺苷含量(842.5±173.7 pm ol/mL)与对照组(888.2±273.0 pm ol/mL)相比差异无显著性(P=0.77)。多巴酚丁胺负荷试验后,对照组冠状静脉血浆腺苷含量(1273.0±247.1 pm ol/mL)明显高于静息状态(P<0.05);实验组冠状静脉血浆腺苷含量(950.8±223.0 pm ol/mL)与静息状态相比差异无显著性(P=0.45)。心肌组织腺苷A1受体mRNA相对积分光密度值两组之间差异无显著性。结论:心脏负荷增加时实验组冠状静脉内腺苷处于低水平可能是TMLR缓解心绞痛的机制。     

轻度低氧血症的慢性阻塞性肺疾病患者的心脏结构及功能的早期变化

目的:评估正常动脉血氧分压和无右心室衰竭迹象的慢性阻塞性肺疾病(COPD)患者心脏结构和功能.方法:25个COPD稳定期的患者(FEV1,1.23±0.52 L/s;PaO2,82±10 mm Hg),26个与研究对象年龄匹配的受试者作为对照组.以超声多普勒超声心动图测定右心室(RV)和左心室(LV)的结构与功能及检肺动脉压(PAP).结果:COPD组与对照组右心室舒张期末直径为19±3mm,23±2mm,(P＜0.01),三尖瓣口舒张期血流速度比值为1.2±0.9,1.5±0.4(P＜0.05);右心室壁舒张末期厚度为4±0.9,3±0.8,(P＜0.05);右心室射血分数56±12,60±11(P＞0.05).COPD组与对照组左心室舒张期直径为48.0±5.5,46.2±3.4(P＞0.05);二尖瓣口舒张期血流速度比值:1.2±0.4,1.5±0.9左心室后壁厚度为10.0±0.8,10.3±0.7(P＞0.05);EF斜率55.5±11.7,54.5±12.1(P＞0.05);左室舒张早期最大充盈速率分数为2.83±0.43,2.81±0.45 (P＞0.05);左心室射血分数53±7,62±14(P＞0.05);COPD组与对照组均不伴有肺动脉高压.结论:心肌肥厚是COPD患者右心室压力超负荷最早迹象,这些心脏的适应性变化不改变左右心室的收缩功能.     

低氧对大鼠右心室肥厚及心肌中缝隙连接蛋白43表达的影响

目的:研究低氧对大鼠右心室肥厚及心肌中缝隙连接蛋白43 (Cx43)表达的影响.方法:40只健康雄性SD大鼠随机分为正常组(control)、低氧3周组、低氧4周组和低氧5周组.除正常组外,其余3组大鼠分别在低氧环境中饲养3周、4周和5周.测定和比较各组大鼠的平均肺动脉压力(mPAP)、右心室收缩压(RVSP)、右心室肥厚度[Rv/(LV+S)％],并通过免疫组化染色法观察各组大鼠左心室心肌细胞中cx43的表达.结果:与正常组相比,低氧3周、4周、5周组大鼠的mPAP、RVSP、右心室肥厚度均显著升高(P均＜0.05),与低氧3周组比较,低氧4周、5周组大鼠的mPAP、RVSP、右心室肥厚度均显著升高(P均＜0.05),而低氧5周组大鼠的mPAP、RVSP、右心室肥厚度均显著高于低氧4周(P均＜0.05).免疫组织化学结果显示:低氧组大鼠Cx43排列紊乱,端-端连接减少,侧面连接增多;随着低氧时间的延长,大鼠心肌细胞中Cx43的表达逐渐减少,差异具有统计学意义(P均＜0.05).结论:低氧可导致右心室肥厚,并随着诱导时间的延长而逐渐加重,这可能与心肌中Cx43的分布紊乱及表达减少有关.     

高脂高糖饮食对自发性高血压大鼠腹主动脉舒张功能及VCAM-1和ICAM-1mRNA表达的影响

目的:探讨高脂高糖饮食对自发性高血压大鼠(spontaneously hypertensive rats,SHR)腹主动脉血管舒张功能及血管间粘附分子-1 (vascular adhesion molecule-1,VCAM-1)和细胞间粘附分子-1(intercellular adhesion molecule-1,ICAM-1)mRNA表达的影响.方法:将24只6周龄雄性SHR大鼠随机分成高脂高糖饲料组(实验组,n=12)和普通饲料组(对照组,n=12).每3周测量其空腹体重,12周后处死大鼠,分别取两组动物的腹主动脉做离体血管环对乙酰胆碱(Acetylcholine,Ach)的舒张功能实验,并提取主动脉总RNA,通过实时定量RT-PCR实验检测其VCAM-1和ICAM-1 mRNA的表达.结果:从第6周开始,实验组SHR的体重较对照组明显增加(P＜0.01).12周时,实验组血管环对Ach的最大舒张率较对照组明显降低(69.20± 5.25 vs.79.10± 3.84,P＜0.01);实验组动脉VCAM-1 mRNA的相对表达量是对照组的1.97倍,差异有统计学意义(197.91±22.16 vs.100.33±11.44,P＜0.01),而两组ICAM-1mRNA表达的比较差异无统计学意义(97.75±8.05 vs.100.25±10.83,P＞0.05).结论:高脂高糖饮食能致SHR腹主动脉血管舒张功能明显降低,可能与其显著增加其主动脉VCAM-1 mRNA的表达有关.     

氟桂利嗪联合血塞通治疗偏头痛患者的临床疗效及对血液流变学的影响

目的:探讨氟桂利嗪联合血塞通治疗偏头痛患者的临床疗效及对血液流变学的影响。方法:选择2012年2月到2014年6月在我院就诊的240例偏头痛患者,随机分为对照组(n=120)和实验组(n=120)。对照组给予氟桂利嗪治疗,实验组在对照组基础上加用血塞通治疗,对比两组治疗效果和治疗前后血液流变学的变化。结果:治疗后两组患者偏头痛发作频率及VAS评分较治疗前均显著降低(P0.05),疼痛持续时间显著缩短(P0.05)且实验组显著优于对照组(P0.05);实验组的有效率(95.8%)明显高于对照组(72.5%),具有显著性差异(P0.05)。治疗后两组患者血浆黏度、全血高、低切黏度、红细胞压积及纤维蛋白原较治疗前均显著降低(P0.05),且实验组患者各指标均显著低于对照组(P0.05)。结论:氟桂利嗪联合血塞通治疗偏头痛临床疗效显著,可显著改善患者血液流变学指标,效果优于单独使用氟桂利嗪。     

Automated Axial Right Ventricle to Left Ventricle Diameter Ratio Computation in Computed Tomography Pulmonary Angiography

ResultsThe CAD system analyzed correctly 92.4% (183/198) of CTPA studies. The mean difference between automated and manually computed axial RV/LV ratios was 0.03±0.22. The correlation between the RV/LV diameter ratio obtained by the CAD system and that obtained by the radiologist was high (r=0.81). Compared to the radiologist, the CAD system equally achieved high accuracy for the composite outcome, with areas under the receiver operating characteristic curves of 0.75 vs. 0.78. Similar results were found for 30-days PE-specific mortality, with areas under the curve of 0.72 vs. 0.75.ConclusionsAn automated CAD system for determining the CT derived RV/LV diameter ratio in patients with acute PE has high accuracy when compared to manual measurements and similar prognostic significance for two clinical outcomes.     

Adipokines and the Right Ventricle: The MESA-RV Study

Objective

Obesity is associated with changes in both right (RV) and left (LV) ventricular morphology, but the biological basis of this finding is not well established. We examined whether adipokine levels were associated with RV morphology and function in a population-based multiethnic sample free of clinical cardiovascular disease.

Methods

We examined relationships of leptin, resistin, TNF-α, and adiponectin with RV morphology and function (from cardiac MRI) in participants (n = 1,267) free of clinical cardiovascular disease from the Multi-Ethnic Study of Atherosclerosis (MESA)-RV study. Multivariable regressions (linear, quantile [25^th and 75^th] and generalized additive models [GAM]) were used to examine the independent association of each adipokine with RV mass, RV end-diastolic volume (RVEDV), RV end-systolic volume (RVESV), RV stroke volume (RVSV) and RV ejection fraction (RVEF).

Results

Higher leptin levels were associated with significantly lower levels of RV mass, RVEDV, RVESV and stroke volume, but not RVEF, after adjustment for age, gender, race, height and weight. These associations were somewhat attenuated but still significant after adjustment for traditional risk factors and covariates, and were completely attenuated when correcting for the respective LV measures. There were no significant interactions of age, gender, or race/ethnicity on the relationship between the four adipokines and RV structure or function.

Conclusions

Leptin levels are associated with favorable RV morphology in a multi-ethnic population free of cardiovascular disease, however these associations may be explained by a yet to be understood bi-ventricular process as this association was no longer present after adjustment for LV values. These findings complement the associations previously shown between adipokines and LV structure and function in both healthy and diseased patients. The mechanisms linking adipokines to healthy cardiovascular function require further investigation.     

Right Ventricular Morphology and the Onset of Dyspnea: The MESA-Right Ventricle Study

Background

The association of right ventricular (RV) structure and function with symptoms in individuals without cardiopulmonary disease is unknown. We hypothesized that greater RV mass and RV end-diastolic volume (RVEDV), smaller RV stroke volume (RVSV), and lower RV ejection fraction (RVEF) measured by cardiac magnetic resonance imaging (MRI) in participants free of clinical cardiovascular disease at baseline would be associated with a greater risk of self-reported dyspnea.

Methods

The Multi-Ethnic Study of Atherosclerosis (MESA) performed cardiac MRIs on participants without clinical cardiovascular disease between 2000 and 2002. We excluded subjects who reported “prevalent” dyspnea at the first assessment (24 months). The presence of dyspnea was assessed at 24 months, 42 months, and 60 months from baseline. Cox proportional hazards models were used to examine the relationship between RV measures and incident dyspnea.

Results

In the final study sample (N = 2763), there were significant interactions between RV measures and sex in terms of the risk of dyspnea (p<0.05). Among men (N = 1453), lower RV mass (p = 0.003), smaller RVEDV (p<0.001), smaller RV end-systolic volume (RVESV) (p = 0.03) and decreased RVSV (p<0.001) were associated with an increased risk of developing dyspnea after adjusting for covariates. Associations remained after adjusting for left ventricular function and lung function. However, there were no significant associations between RV measures and the risk of dyspnea in women.

Conclusions

Lower RV mass and smaller RV volumes were associated with an increased risk of dyspnea in men, but not in women.     

Real-Time Three-Dimensional Echocardiography to Assess Right Ventricle Function in Patients with Pulmonary Hypertension

Background

The convenience and availability of real-time three-dimensional echocardiography (RT3DE) makes it an attractive candidate for assessing right ventricle function. However, the viability of RT3DE is not conclusive.

Aim of Study

This study aims to evaluate RT3DE relative to cardiac magnetic resonance and 2-dimensional echocardiography (2DE) for measuring right ventricular systolic function in patients with pulmonary hypertension.

Methods

Patients with pulmonary hypertension (n = 23) underwent cardiac magnetic resonance, 2DE, and RT3DE. Specifically, 2DE was used to measure the right ventricular index of myocardial performance (RIMP), fractional area change, tricuspid annular plane systolic excursion (TAPSE), and tissue Doppler-derived tricuspid annular systolic velocity (S′). Cardiac magnetic resonance and RT3DE were used to measure right ventricular end-diastolic volume (RVEDV) and end-systolic volume (RVESV). The right ventricular ejection fraction (RVEF) was calculated.

Results

Regarding the measurements taken by 2DE, RVEF positively correlated with fractional area change (r = 0.595, P = 0.003) and S′(r = 0.489, P = 0.018), and negatively correlated with RIMP (r = −0.745, P = 0.000). There was no association between RVEF and TAPSE (r = −0.029, P = 0.896). There existed a close correlation between the values of RVEDV, RVESV, and RVEF as measured by RT3DE and CMR respectively (P<0.001); Bland-Altmanan analyses showed good agreement between them.

Conclusion

RT3DE was a viable method for noninvasive, accurate assessment of right ventricular systolic function in patients with pulmonary hypertension.     

CFC1 Mutations in Patients with Transposition of the Great Arteries and Double-Outlet Right Ventricle

Recent investigations identified heterozygous CFC1 mutations in subjects with heterotaxy syndrome, all of whom had congenital cardiac malformations, including malposition of the great arteries. We hypothesized that a subset of patients with similar types of congenital heart disease---namely, transposition of the great arteries and double-outlet right ventricle, in the absence of laterality defects---would also have CFC1 mutations. Our analysis of the CFC1 gene in patients with these cardiac disorders identified two disease-related mutations in 86 patients. The present study identifies the first autosomal single-gene defect for these cardiac malformations and indicates that some cases of transposition of the great arteries and double-outlet right ventricle can share a common genetic etiology with heterotaxy syndrome. In addition, these results demonstrate that the molecular pathway involving CFC1 plays a critical role in normal and abnormal cardiovascular development.