This study was supported by NIH grants HL091986 (JPD) and HL094692 (MTZ).

注:此动物议定书批准的机构动物护理和使用委员会（IACUC）在俄亥俄州立大学。此过程可用于在任何小鼠中，在颈动脉的内径大到足以插入导管。用小鼠是超过16克（超过〜2个月）。 1.准备鼠标导尿<ol><li>密封所有手术器械和用品的消毒袋。消毒在高压釜中的机器的小袋。保持整个过程的无菌区域和戴无菌手套。 </li><li>麻醉小鼠用氯胺酮（55毫克/千克）加赛拉嗪（15毫克/千克）通过腹膜内注射。 注:整个过程同时测量压力/容积在不同的心脏速率和ESPRV只需要不到20分钟。如果需要额外的时间（ 即 ，超过30分钟以上），得到另外¼剂量麻醉的每30分钟。 </li><li>除去毛在前ř颈部和胸部区域使用毛发去除洗剂（ 例如 ，奈尔）和egion胶带将小鼠的肢体上的泡沫平台。由脚趾捏确认深度麻醉状态。 </li><li>插入直肠探针监测体温（37±1℃），并保持使用热调节的加热垫（位于外科被单和平台之间）。 </li><li>准备4-0缝合线（约10厘米）长。绕上门牙环缝合带与平台。这将保持颈部挺直。 </li><li>通过擦拭用聚维酮碘和75％乙醇的三倍区域消毒的手术区域。 </li></ol> 2.导尿<ol><li>通过预浸泡的尖端在盐水或蒸馏水（37℃）至少30分钟制备的导管使用（根据制造商的说明），以适应新环境的压力传感器膜片的湿生物环境和防止压力信号漂移和负前压力记录。 </li><li>使下颚和胸骨在颈部的前部区域之间的纵向0.8厘米切口。随着精剪，分离皮肤，肌肉结缔组织揭露设下的肌肉stemohyoideus气管。 </li><li>在右侧与弯钳气管分离脂肪和肌肉组织以暴露右颈动脉。 注:颈动脉是颈部前区最大的动脉，包含了鲜红的血，是搏动。不要混淆与平行延伸到颈动脉颈内静脉。颈静脉是暗红色和非搏动。此外，在颈动脉的隔离期间，用户应该意识到不损害迷走神经的。 </li><li>从右颈动脉与弯曲镊子去除脂肪。如果存在分支，这将阻碍该操作技术的船只，切断他们与bovie刀烧灼分离颈动脉。分离尽可能多的组织尽可能使用弯钳颈动脉之下。 </li><li>切两5厘米6-0丝线。通过右颈总动脉下的每个丝线。 </li><li>位置一个线程邻近近端部分和其他邻近动脉的远端部分。使线程上紧结在远端部分，并且使线程上的松散的结在近端部分。 </li><li>通过夹紧用小止血血管钳动脉的近端部分阻塞血流（将近端螺纹下方的夹具）。动脉的密封区域将充满血液使其易于执行步骤2.8。 </li><li>穿刺一个小孔在两个线程（但更靠近所述远端螺纹）之间的右颈动脉用一个＆G针。插入导管插入颈动脉。略微收紧松散结在颈动脉的近端部分上的导管保持在适当位置。 注:使用穿刺是首选比较剪刀切口。通过使紧结在动脉的远端部分，然后再夹紧近端部分，动脉将被完全充满血液。这使得它非常容易捅血管。此外，该针（26 G）的大小穿刺与很好地配合在导管的尺寸的孔的动脉。当使用剪刀切口的方法，它是更加难以控制切口的大小。但是，选择的方法应该是取决于哪一个外科医生感觉更舒服。 </li><li>开始录制的压力信号，在第3步。 </li><li>松开止血钳，继续向前插入导管进入左心室。如果推进导管当一些阻力经历，轻轻拉回来，然后再试一次推进。对于一个小鼠体重〜18-25克，所插入的导管的估计长度为18毫米。 注:动脉压信号会波动从70至120毫米汞柱。一旦牛逼他导管是在左心室的压力信号的变化的形状和压力会波动，从0到120毫米汞柱（ 图1中示出）。心脏功能将插入导管后的2-3分钟稳定。 </li><li>连续监测体温，麻醉水平，和呼吸率。 </li></ol> 3.数据采集<ol><li>使用LabChartPro 7软件（或类似软件）。使用PV环LabChart模块的工作流程选项。使用此模块中，选择压力和容积循环默认设置。 </li><li>建立三个通道:一个通道的压力，一个通道音量，和一个通道对心脏率。以上参数为0-150毫米汞柱，0-100微升和0-800次/分钟，分别设定量程范围。 </li><li>按开始键记录。 </li></ol> 4.鲍迪奇影响<ol><li>制成1厘米的切口平行于所述柄的心前区面积。切断肌肉和EXP层OSE的肋间用剪刀。 </li><li>采用方波脉冲刺激，设置以下参数:电压为2 V，2毫秒的时间，并启用重复模式。 </li><li>握住钳子负极，并通过第四肋间隙心脏的心尖区插入。持用钳子的正极，并通过第二肋间到心脏的右心房区域插入。 </li><li>打开刺激器，改变频率，从4赫兹（240次/分）起搏心脏高达10赫兹（600次/分）。在每一个新的心脏率，刺激心脏进行数据采集前1分钟。 </li></ol> 5.生成ESPVR和PRSW <ol><li>切开皮肤和肌肉组织垂直于用剪刀腹部区域的柄。打开enterocoelia并露出肝脏。 </li><li>拖动弓costarum朝向头部采用金属牵引。 </li><li>轻轻地向下肝脏与推棉签。小心不要推太多影响胸腔。这将改变心脏功能。 </li><li>割肝的镰状韧带用剪刀以暴露肝上下腔静脉（IVC）。 </li><li>用弯钳迅速挤压下腔静脉，持续5秒，以阻断血液回流到右心房。左心室压力和容积将下降，由于减少了流入到心脏。在产生这些值，不要使用低于60毫米汞柱循环。 60毫米汞柱是在参考收缩压。 注意:此值被设定为60毫米汞柱，因为这将导致在灌注压一个显著下降到显着降低冠状动脉灌注和影响收缩力。 </li></ol> 6.音量校正<ol><li> Heparinize的小鼠用0.1ml的1:5000肝素溶液（用生理盐水稀释）通过腹膜内注射。 </li><li>从颈动脉取出导管。当导管被拉出FR嗡颈动脉，肝素化血液会渗入从插入导管，其中该孔。 </li><li>收集这些血用1毫升注射器体积校准。每个校准比色皿井填。 </li><li>删除通过心脏放血安乐死鼠标。 </li><li>定位在每个导管孔，并获得稳定的相对体积单元（RVU）值。生成使用各种标准体积和RVU值从每个孔的标准曲线。 </li><li>转换录制的RVU到微升。 </li></ol> 7.数据处理<ol><li>为了检验效果鲍迪奇，从每个心脏率稳态压力/体积的痕迹。点击基线分析，以获得数据。 </li><li>对于ESPVR和PRSW数据，选择第一〜15压力/容积痕迹，单击闭塞分析软件来生成ESPVR和PRSW（用在LV舒张末期容积形成的压力的斜率）（工作行程的线性回归与舒张末期体积）的斜坡。 </li><li>兼顾环的形状。确保环没有角点或曲折关闭。这是不正确的导管放置或噪声过大的迹象。在实验过程中定期检查循环，以确保正在生成适当的压力和体积数据。 </li></ol>

<ol>
	<li>Janssen, P. M. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Myocardial+contraction-relaxation+coupling.">Myocardial contraction-relaxation coupling.</a> Am J Physiol Heart Circ Physiol. 299, H1741-H1749 (2010).</li><li>Roman, M. J., Devereux, R. B. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Comparison+of+noninvasive+measures+of+contractility+in+dilated+cardiomyopathy.">Comparison of noninvasive measures of contractility in dilated cardiomyopathy.</a> Echocardiography. 8, 139-150 (1991).</li><li>Hamlin, R. L., del Rio, C. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=dP/dt(max)--a+measure+of+'baroinometry.">dP/dt(max)--a measure of 'baroinometry.</a> J Pharmacol Toxicol Methods. 66, 63-65 (2012).</li><li>Feneley, M. P., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Comparison+of+preload+recruitable+stroke+work,+end-systolic+pressure-volume+and+dP/dtmax-end-diastolic+volume+relations+as+indexes+of+left+ventricular+contractile+performance+in+patients+undergoing+routine+cardiac+catheterization.">Comparison of preload recruitable stroke work, end-systolic pressure-volume and dP/dtmax-end-diastolic volume relations as indexes of left ventricular contractile performance in patients undergoing routine cardiac catheterization.</a> J Am Coll Cardiol. 19, 1522-1530 (1992).</li><li>Kass, D. A., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Comparative+influence+of+load+versus+inotropic+states+on+indexes+of+ventricular+contractility:+experimental+and+theoretical+analysis+based+on+pressure-volume+relationships.">Comparative influence of load versus inotropic states on indexes of ventricular contractility: experimental and theoretical analysis based on pressure-volume relationships.</a> Circulation. 76, 1422-1436 (1987).</li><li>Nemoto, S., DeFreitas, G., Mann, D. L., Carabello, B. A. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Effects+of+changes+in+left+ventricular+contractility+on+indexes+of+contractility+in+mice.">Effects of changes in left ventricular contractility on indexes of contractility in mice.</a> Am J Physiol Heart Circ Physiol. 283, H2504-H2510 (2002).</li><li>Ziolo, M. T., Kohr, M. J., Wang, H. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Nitric+oxide+signaling+and+the+regulation+of+myocardial+function.">Nitric oxide signaling and the regulation of myocardial function.</a> J Mol Cell Cardiol. 45, 625-632 (2008).</li><li>Barouch, L. A., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Nitric+oxide+regulates+the+heart+by+spatial+confinement+of+nitric+oxide+synthase+isoforms.">Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms.</a> Nature. 416, 337-339 (2002).</li><li>Wang, H., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=Neuronal+nitric+oxide+synthase+signaling+within+cardiac+myocytes+targets+phospholamban.">Neuronal nitric oxide synthase signaling within cardiac myocytes targets phospholamban.</a> Am J Physiol Cell Physiol. 294, C1566-C1575 (2008).</li><li>Georgakopoulos, D., et al. <a target="_blank" href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=PubMed&cmd=Search&doptcmdl=Citation&defaultField=Title+Word&term=In+vivo+murine+left+ventricular+pressure-volume+relations+by+miniaturized+conductance+micromanometry.">In vivo murine left ventricular pressure-volume relations by miniaturized conductance micromanometry.</a> Am J Physiol. 274, H1416-H1422 (1998).</li></ol>

There are no competing financial interests.

此技术获得收缩的可靠措施的一个关键步骤是正确的导管放置到LV。如果导管被放置不正确，当左心室收缩的壁可接触导致非常高的，而不是生理，压力值造成的不规则形状的PV循环导管。如果需要的话，该导管可以旋转以实现正确的放置。这种技术的另一个关键步骤是确保鼠标得到适当的麻醉。如果鼠标在麻醉，这将大大降低心脏功能。鼠标与心脏率低于〜250次/分，可考虑在麻醉。此外，采血?...

心脏的目的是泵整个身体的血液满足微生物的代谢需求。由于这些要求都在不断波动（ 例如 ，运动时），心脏必须适应（ 即 ，增加心输出量）。心脏有无数的设计途径来完成这一壮举。黄金的方式达到心脏，这是通过增加心脏率（ 即 ，鲍迪奇效果）1。即，当一个人的心脏速率增加，这导致增加的收缩力，并增加了心输出量。因此，心脏功能极其取决于心脏率。不幸的是，心脏疾病（ 例如 ，心肌梗塞，肥大等 ）导致低劣的心脏功能，其中心脏因此将不能满足身体的代谢需要。心脏疾病是发病率和死亡率在西方社会的主要病因。该重述许多人类cardiomy动物模型opathies被用于研究分子机制和测试潜在疗法。要辨别这些机制，并确定是否治疗可能是可行的，研究者必须评估在体内的心脏功能。 有几种方法来评估心脏功能的体内 （ 例如 ，超声心动图，MRI 等 ），这经常测量射血分数，缩短分数，心输出量， 等等。然而，这些参数是高度依赖于后负荷，预压，和心脏速率除了 ​​收缩2。测量收缩是必不可少的在其原生环境中领悟心脏的内在属性。最大（DP / dt 最大值 ）率压力的发展使我们更接近了一步了解收缩。不幸的是，上升/ dt为还取决于心脏速率和负载条件3。因此技术已被开发用于测量负载（和心脏速率，参见贝尔流）心肌收缩力指数无关（ 即 ，收缩末期容积压力的关系（ESPVR）和预紧recruitable工作行程（PRSW））4-6。 ESPVR描述了可以通过心室在任何给定的LV体积要开发的最大压力。 ESPVR的斜率代表收缩末期弹性（EES）。 PRSW是脑卒中工作（由PV环封闭区域）与舒张末期容积的线性回归。这些程序是收缩的更准确和精确的测量相比的血流动力学参数，如射血分数，心输出量，和每搏输出量。 ESPVR和PRSW可以经由下腔静脉（IVC）的临时阻塞而获得。阻断IVC可以带有闭合胸腔进行，以避免改变对心脏功能胸膜内压力的作用。 增加心脏率也提高了收缩和舒张1。因此，比较experimenta之间心脏功能时，L基团（ 如 ±DP / DT），心脏率必须相似。但是，类似的心脏率通常不因各种条件（疾病，研究干预等 ）发生在每个动物。应当指出的是，麻醉（注射和吸入）降低心脏速率。作为心脏速率是收缩的主要决定因素，麻醉将大大影响收缩力。出于这个原因，我们描述我们的程序。此外，许多心肌病的特点是降低收缩储备（ 即降低鲍迪奇效应）。因此，心脏功能应测在一系列心脏率。这里，我们描述了如何使用一个刺激（带有闭合胸腔）来实现这些效果。 除了 ​​心脏速率，一氧化氮（NO）也是收缩7的重要调节剂。否是通过生产的酶称为NO合成酶（NOS）。我们和其他人已经表明，小鼠神经元NOS的基因敲除（NOS1 <s达&gt; - / - ）已经减弱心肌细胞在体内的心脏血流动力学8,9收缩。该小鼠将用于经由在不同的心脏速率执行的低压压力/体积分析程序来演示的左心室收缩测量。

<table><tbody><tr><td>Xlyzine 100&amp;nbsp;mg/ml</td><td>Ana Sed</td><td>4821</td><td></td></tr><tr><td>Katamin 50&amp;nbsp;mg/ml</td><td>Ketalar</td><td>310006</td><td></td></tr><tr><td>Heparin</td><td>APP Pharmaceuticals</td><td>6003922</td><td></td></tr><tr><td>4-0 silk thread</td><td>Surgical specialties</td><td>SP102</td><td></td></tr><tr><td>6-0 silk thread</td><td>Surgical specialties</td><td>MBKF270</td><td></td></tr><tr><td>Forceps</td><td>Fine Science Tools</td><td>11251-10</td><td></td></tr><tr><td>Curve forceps</td><td>Fine Science Tools</td><td>11274-20</td><td></td></tr><tr><td>Scissors</td><td>Fine Science Tools</td><td>14090-09</td><td></td></tr><tr><td>Vascular clamp</td><td>Fine Science Tools</td><td>18555-03</td><td></td></tr><tr><td>Microscope</td><td>World precision instruments</td><td>PZM-3</td><td></td></tr><tr><td>Pressure catheter</td><td>Millar instruments</td><td>SPR-839</td><td></td></tr><tr><td>Pressure and volume system</td><td>Millar instruments</td><td>MPVS-300</td><td></td></tr><tr><td>PowerLab4/35</td><td>AD instruments</td><td>N12128</td><td></td></tr><tr><td>LabchartPro 7</td><td>AD instruments</td><td></td><td></td></tr><tr><td>Temperature controller</td><td>CWE</td><td>TC-1000</td><td></td></tr><tr><td>Stimulator</td><td>Grass</td><td>SD-5</td><td></td></tr><tr><td>Sterile glove</td><td>Micro-Touch</td><td>1305018821</td><td></td></tr><tr><td>Hair remover lotion</td><td>Nair</td><td></td><td></td></tr><tr><td>Betadine surgical scrub</td><td>Veterinary</td><td>NDC 6761815401</td><td></td></tr><tr><td>Alcohol</td><td>Decon Laboratories</td><td>2801</td><td></td></tr><tr><td>Bovie cautery</td><td>Bovie</td><td>AA29</td><td></td></tr><tr><td>1&amp;nbsp;ml Syringe (26&amp;nbsp;G needle)</td><td>BD</td><td>8017299</td><td></td></tr></tbody></table>

cardiac catheterization in mice to measure the pressure volume relationship: investigating the bowditch effect

已创建模仿人类心脏疾病的动物模型来测试潜在的治疗策略。一个关键组成部分，以评估这些战略是考察其对心脏功能的影响。有几种技术在体内心脏力学（ 例如 ，超声心动图，压力/容积关系， 等等 ）来衡量。相比超声心动图，经由导管左实时左心室（LV）的压力/体积分析更精确，见地在评估LV功能。此外，LV压力/体积分析提供了在收缩（ 如 β肾上腺素能刺激）和病理损伤（ 如缺血/再灌注损伤）的操作来记录瞬间变化的能力。除了 ​​最大值（+ DP / dt）的和最小（-dP / dt）的压力变化在LV速率，LV功能通过多个负载无关的索引的准确评估（ 例如 ，收缩末压力体积的关系和预紧recruitable行程工作）可以实现。心脏速率对左心室收缩一个显著效果，使得增加的心脏速率是提高心输出量（ 即 ，鲍迪奇效应）的主要机制。因此，实验组之间比较血流动力学时，有必要具有类似心脏速率。此外，许多病车型的标志是在收缩储备的减少（ 即减少鲍迪奇效果）。因此，重要的信息可以通过确定增加心脏速率上收缩的影响而获得。我们和其他人的数据表明，神经元型一氧化氮合酶（NOS1）基因敲除小鼠已减少收缩。在这里，我们描述了测量左室压力/体积随用NOS1基因敲除小鼠模型心脏率的过程。

正常插入导管进入左心室是达到适当的压力和体积值的一个重要步骤。 如图1中所示，使用LabChart Pro 7中，是压力波形（形状和值）作为导管的推移从动脉进入心室的变化。 正确插入导管进入左心室后，将压力（P）和体积（V）中得到将被用来产生光伏回路的值（示于图2）。 利用这些压力值，从而改变收缩机制可以进行调查。 <st...

Watch this Scientific Journal Video about Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect at JoVE.com

Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect

This article describes the measurement of murine left ventricular function via pressure/volume analysis at different heart rates.

心导​​管在小鼠测量压力体积的关系:调查的影响鲍迪奇

Animal models that mimic human cardiac disorders have been created to test potential therapeutic strategies. A key component to evaluating these ...

cardiac-catheterization-mice-to-measure-pressure-volume-relationship

Research

JoVE Journal

Medicine

18.0K 次观看.  The Ohio State University. This article describes the measurement of murine left ventricular function via pressure/volume analysis at different heart rates.

视频: Cardiac Catheterization in Mice to Measure the Pressure Volume Relationship: Investigating the Bowditch Effect

Permanent Ligation of the Left Anterior Descending Coronary Artery in Mice: A Model of Post-myocardial Infarction Remodelling and Heart Failure

Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with cellular oxygen requirements at rest or during stress. It is characterized by fluid retention, shortness of breath, and fatigue, in particular on exertion. Heart failure is a growing public health problem, the leading cause of hospitalization, and a major cause of mortality. Ischemic heart disease is the main cause of heart failure.
Ventricular remodelling refers to changes in structure, size, and shape of the left ventricle. This architectural remodelling of the left ventricle is induced by injury (e.g., myocardial infarction), by pressure overload (e.g., systemic arterial hypertension or aortic stenosis), or by volume overload. Since ventricular remodelling affects wall stress, it has a profound impact on cardiac function and on the development of heart failure. A model of permanent ligation of the left anterior descending coronary artery in mice is used to investigate ventricular remodelling and cardiac function post-myocardial infarction. This model is fundamentally different in terms of objectives and pathophysiological relevance compared to the model of transient ligation of the left anterior descending coronary artery. In this latter model of ischemia/reperfusion injury, the initial extent of the infarct may be modulated by factors that affect myocardial salvage following reperfusion. In contrast, the infarct area at 24 hr after permanent ligation of the left anterior descending coronary artery is fixed. Cardiac function in this model will be affected by 1) the process of infarct expansion, infarct healing, and scar formation; and 2) the concomitant development of left ventricular dilatation, cardiac hypertrophy, and ventricular remodelling.
Besides the model of permanent ligation of the left anterior descending coronary artery, the technique of invasive hemodynamic measurements in mice is presented in detail.

Heart failure is the leading cause of hospitalization and a major cause of mortality. A model of permanent ligation of the left anterior descending coronary artery in mice is applied to investigate ventricular remodelling and cardiac dysfunction post-myocardial infarction. The technique of invasive hemodynamic measurements in mice is presented.

左冠状动脉前降支的小鼠结扎:对心肌梗死后重塑和心衰模型

Heart failure is a syndrome in which the heart fails to pump blood at a rate commensurate with cellular oxygen requirements at rest or during stress. It ...

科研

医学

Real-time Pressure-volume Analysis of Acute Myocardial Infarction in Mice

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any potential therapeutic approach directed against acute left ventricular (LV) dysfunction. Current imaging modalities (e.g., echocardiography and magnetic resonance imaging) have several limitations since data on LV pressure cannot directly be measured. LV catheterization in mice undergoing coronary artery occlusion could serve as a novel method for a real-time evaluation of LV function.
At the beginning of the procedure, mice were anesthetized followed by endotracheal intubation. For LV catheterization, the right carotid artery was exposed via middle-neck incision. The catheter was introduced and placed into the LV cavity. Left thoracotomy was conducted and the left main coronary artery (LCA) was ligated. To induce reperfusion, the suture was released after 45 min. Pressure-volume data was recorded at all times.
Ligation of the LCA caused a decrease in LV systolic function as evidenced by a 30% reduction in stroke volume, LV ejection fraction (EF), and cardiac output. Maximum dP/dt as a parameter for LV contractility was also significantly reduced and diastolic function was severely impaired (minimum dP/dt -40%). Reperfusion over a period of 20 min did not lead to a complete recovery of LV function.
Real-time pressure-volume analysis served as a valid procedure for monitoring cardiac function during acute myocardial infarction in mice. Maintaining stable anesthesia and a standardized surgical approach was crucial to ensure valid results. As the early phase of acute myocardial infarction is critical for morbidity and mortality, the delineated method could be beneficial for preclinical evaluation of new strategies for cardioprotection.

Acute myocardial infarction in mice induces acute but incompletely characterized changes in left ventricular (LV) function. LV catheterization in mice undergoing coronary artery occlusion serves as a novel method for a real-time evaluation of LV function.

小鼠急性心肌梗死的实时压力容积分析

Acute myocardial infarction can lead to acute heart failure and cardiogenic shock. The evaluation of hemodynamics is critical for the evaluation of any ...

Invasive Hemodynamic Assessment for the Right Ventricular System and Hypoxia-Induced Pulmonary Arterial Hypertension in Mice

Pulmonary arterial hypertension (PAH) is a chronic and severe cardiopulmonary disorder. Mice are a popular animal model used to mimic this disease. However, the evaluation of right ventricular pressure (RVP) and pulmonary artery pressure (PAP) remains technically challenging in mice. RVP and PAP are more difficult to measure than left ventricular pressure because of the anatomical differences between the left and right heart systems. In this paper, we describe a stable right heart hemodynamic measurement method and its validation using healthy and PAH mice. This method is based on open-chest surgery and mechanical ventilation support. It is a complicated procedure compared to closed chest procedures. While a well-trained surgeon is required for this surgery, the advantage of this procedure is that it can generate both RVP and PAP parameters at the same time, so it is a preferable procedure for the evaluation of PAH models.

Here, we present a protocol to perform an invasive hemodynamic assessment of the right ventricle and pulmonary artery in mice using an open-chest surgery approach.

小鼠右心室系统及缺氧诱发肺动脉高血压的侵入性血液动力学评估

Pulmonary arterial hypertension (PAH) is a chronic and severe cardiopulmonary disorder. Mice are a popular animal model used to mimic this disease. ...

Quantification of Biventricular Function and Morphology by Cardiac Magnetic Resonance Imaging in Mice with Pulmonary Artery Banding

Right ventricular (RV) function and failure are major determinants of outcome in acquired and congenital heart diseases, including pulmonary hypertension. Assessment of RV function and morphology is complex, partly due to the complex shape of the RV. Currently, cardiac magnetic resonance (CMR) imaging is the golden standard for noninvasive assessment of RV function and morphology. The current protocol describes CMR imaging in a mouse model of RV pressure load induced by pulmonary artery banding (PAB). PAB is performed by placing a 6-0 suture around the pulmonary artery over a 23 G needle. The PAB gradient is determined using echocardiography at 2 and 6 weeks. At 6 weeks, the right and left ventricular morphology and function is assessed by measuring both end-systolic and end-diastolic volumes and mass by ten to eleven cine slices 1 mm thick using a 9.4 T magnetic resonance imaging scanner equipped with a 1,500 mT/m gradient. Representative results show that PAB induces a significant increase in RV pressure load, with significant effects on biventricular morphology and RV function. It is also shown that at 6 weeks of RV pressure load, cardiac output is maintained. Presented here is a reproducible protocol for the quantification of biventricular morphology and function in a mouse model of RV pressure load and may serve as a method for experiments exploring determinants of RV remodeling and dysfunction.

To understand the pathophysiology of right ventricular (RV) adaptation to abnormal loading, experimental models are crucial. However, assessment of RV dimensions and function is complex and challenging. This protocol provides a method to perform cardiac magnetic resonance imaging (CMR) as a noninvasive benchmark procedure in mice subjected to RV pressure load.

Right ventricular (RV) function and failure are major determinants of outcome in acquired and congenital heart diseases, including pulmonary hypertension. ...

Biventricular Assessment of Cardiac Function and Pressure-Volume Loops by Closed-Chest Catheterization in Mice

Assessment of cardiac function is essential to conduct cardiovascular and pulmonary-vascular preclinical research. Pressure-volume loops (PV loops) generated by recording both pressure and volume during cardiac catheterization are vital when assessing both systolic and diastolic cardiac function. Left and right heart function are closely related, reflected in ventricular interdependence. Thus, recording biventricular function in the same animal is important to get a complete assessment of cardiac function. In this protocol, a closed chest approach to cardiac catheterization consistent with the way catheterization is performed in patients is adopted in mice. While challenging, the closed chest strategy is a more physiological approach, because opening the chest results in major changes in preload and afterload that create artifacts, most notably a fall in systemic blood pressure. While high-resolution echocardiography is used to assess rodents, cardiac catheterization is invaluable, particularly when assessing diastolic pressures in both ventricles.
Described here is a procedure to perform invasive, closed chest, sequential left and right ventricular pressure-volume (PV) loops in the same animal. PV loops are acquired using&#160;admittance technology with a mouse pressure-volume catheter and pressure-volume system acquisition. The procedure is described, beginning with the neck dissection, which is required to access the right jugular vein and the right carotid artery, to the insertion and positioning of the catheter, and finally the data acquisition. Then, the criteria required to ensure the acquisition of high-quality PV loops are discussed. Finally, the analysis of the left and right ventricular PV loops and the different hemodynamic parameters available to quantify systolic and diastolic ventricular function are briefly described.

Presented here is a protocol to assess biventricular heart function in mice by generating pressure-volume (PV) loops from the right and left ventricle in the same animal using closed chest catheterization. The focus is on the technical aspect of surgery and data acquisition.

小鼠闭胸导管插入术对心功能和压力-容积环的双心室评估

Assessment of cardiac function is essential to conduct cardiovascular and pulmonary-vascular preclinical research. Pressure-volume loops (PV loops) ...

Cardiac Response to &#946;-Adrenergic Stimulation Determined by Pressure-Volume Loop Analysis

Determination of the cardiac function is a robust endpoint analysis in animal models of cardiovascular diseases in order to characterize effects of specific treatments on the heart. Due to the feasibility of genetic manipulations the mouse has become the most common mammalian animal model to study cardiac function and to search for new potential therapeutic targets. Here we describe a protocol to determine cardiac function&#160;in vivo using pressure-volume loop measurements and analysis during basal conditions and under &#946;-adrenergic stimulation by intravenous infusion of increasing concentrations of isoproterenol. We provide a refined protocol including ventilation support taking into account the positive end-expiratory pressure to ameliorate negative effects during open-chest measurements, and potent analgesia (Buprenorphine) to avoid uncontrollable myocardial stress evoked by pain during the procedure. All together the detailed description of the procedure and discussion about possible pitfalls enables highly standardized and reproducible pressure-volume loop analysis, reducing the exclusion of animals from the experimental cohort by preventing possible methodological bias.

Here we describe a cardiac pressure-volume loop analysis under increasing doses of intravenously infused isoproterenol to determine the intrinsic cardiac function and the &#946;-adrenergic reserve in mice. We use a modified open-chest approach for the pressure-volume loop measurements, in which we include ventilation with positive end-expiratory pressure.

通过压力-体积环路分析确定心脏对β肾上腺素能刺激的反应

Determination of the cardiac function is a robust endpoint analysis in animal models of cardiovascular diseases in order to characterize effects of ...

Cardiac Pressure-Volume Loop Analysis Using Conductance Catheters in Mice

Cardiac pressure-volume loop analysis is the &#8220;gold-standard&#8221; in the assessment of load-dependent and load-independent measures of ventricular systolic and diastolic function. Measures of ventricular contractility and compliance are obtained through examination of cardiac response to changes in afterload and preload. These techniques were originally developed nearly three decades ago to measure cardiac function in large mammals and humans. The application of these analyses to small mammals, such as mice, has been accomplished through the optimization of microsurgical techniques and creation of conductance catheters. Conductance catheters allow for estimation of the blood pool by exploiting the relationship between electrical conductance and volume. When properly performed, these techniques allow for testing of cardiac function in genetic mutant mouse models or in drug treatment studies. The accuracy and precision of these studies are dependent on careful attention to the calibration of instruments, systematic conduct of hemodynamic measurements and data analyses. We will review the methods of conducting pressure-volume loop experiments using a conductance catheter in mice.

Cardiac pressure-volume loop analysis is the most comprehensive way to measure cardiac function in the intact heart. We describe a technique to perform and analyze cardiac pressure volume loops, using conductance catheters.

心脏压力容量环分析小鼠使用电导导管

Cardiac pressure-volume loop analysis is the &#8220;gold-standard&#8221; in the assessment of load-dependent and load-independent measures of ventricular ...

生物学

Measuring Pressure Volume Loops in the Mouse

Understanding the causes and progression of heart disease presents a significant challenge to the biomedical community. The genetic flexibility of the mouse provides great potential to explore cardiac function at the molecular level. The mouse&#39;s small size does present some challenges in regards to performing detailed cardiac phenotyping. Miniaturization and other advancements in technology have made many methods of cardiac assessment possible in the mouse. Of these, the simultaneous collection of pressure and volume data provides a detailed picture of cardiac function that is not available through any other modality. Here a detailed procedure for the collection of pressure-volume loop data is described. Included is a discussion of the principles underlying the measurements and the potential sources of error. Anesthetic management and surgical approaches are discussed in great detail as they are both critical to obtaining high quality hemodynamic measurements. The principles of hemodynamic protocol development and relevant aspects of data analysis are also addressed.

This manuscript describes a detailed protocol for the collection of pressure-volume data from the mouse.

测量压力容量环中的鼠标

Understanding the causes and progression of heart disease presents a significant challenge to the biomedical community. The genetic flexibility of the ...

Multiple Intravenous Bolus Dosing and Invasive Hemodynamic Assessment in a Hypoxia-Induced Mouse Pulmonary Artery Hypertension Model

Pulmonary arterial hypertension (PAH) is a progressive life-threatening disease, primarily affecting small pulmonary arterioles of the lung. Currently, there is no cure for PAH. It is important to discover new compounds that can be used to treat PAH. The mouse hypoxia-induced PAH model is a widely used model for PAH research. This model recapitulates human clinical manifestations of PAH Group 3 disease and is an important research tool to evaluate the effectiveness of new experimental therapies for PAH. Research using this model often requires the administration of compounds in mice. For a compound that needs to be given directly into the bloodstream, optimizing intravenous (IV) administration is a key part of the experimental procedures. Ideally, the IV injection system should permit multiple injections over a set time course. Although the mouse hypoxia-induced PAH model is very popular in many laboratories, it is technically challenging to perform multiple IV bolus dosing and invasive hemodynamic assessment in this model. In this protocol, we present step-by-step instructions on how to carry out multiple IV bolus dosing via mouse jugular vein and perform arterial and right ventricle catheterization for hemodynamic assessment in mouse hypoxia-induced PAH model.

This protocol provides a step-by-step procedure for executing multiple intravenous bolus dose administration and invasive hemodynamic monitoring in mice. Investigators can use this protocol for future therapeutic compound screening for pulmonary artery hypertension.

缺氧诱导小鼠肺动脉高压模型中的多次静脉推注给药和侵入性血流动力学评估

Pulmonary arterial hypertension (PAH) is a progressive life-threatening disease, primarily affecting small pulmonary arterioles of the lung. Currently, ...

使用压力-体积电导技术监测大鼠的心脏功能

Real-Time Detection of Ferulic Acid Effects on Rat Left Ventricle Using Pressure-Volume Conductivity Catheter

Decreased cardiac function can have a negative impact on other organs. The left ventricular pressure-volume relationship is considered to be a valid method for evaluating cardiac function. Real-time monitoring of cardiac function is important for drug evaluation. Under closed-chest conditions, the miniature transducer, which is an important component of the pressure-volume catheter, enters the left ventricle of the rat through the right carotid artery. The device visualizes the changes in cardiac function during the experiment in the form of a pressure-volume loop. The actual volume of the ventricle is calculated by altering the conductivity of the blood by injecting 50 &#181;L of a 20% sodium chloride solution into the rat's left jugular vein. The actual volume of the rat's ventricular cavity is calculated by measuring the conductivity of the blood in a known volume using a pressure-volume conductance catheter. This protocol allows for continuous observation of the effects of drugs on the heart and will promote the rationale for the use of specialty ethnic drugs in cardiovascular disease.

作者聚焦：压力-体积环测量方法在心血管研究中的优势

This protocol describes a method for measuring left ventricular pressure and volume using the pressure-volume conductance technique. This method enables continuous real-time monitoring of the effects of drugs on the heart.

使用压力-容积电导导管实时检测阿魏酸对大鼠左心室的影响

Decreased cardiac function can have a negative impact on other organs. The left ventricular pressure-volume relationship is considered to be a valid ...

心导管在小鼠测量压力体积的关系:调查的影响鲍迪奇

摘要

探索更多视频

此视频中的章节

左冠状动脉前降支的小鼠结扎:对心肌梗死后重塑和心衰模型

小鼠急性心肌梗死的实时压力容积分析

小鼠右心室系统及缺氧诱发肺动脉高血压的侵入性血液动力学评估

Quantification of Biventricular Function and Morphology by Cardiac Magnetic Resonance Imaging in Mice with Pulmonary Artery Banding

小鼠闭胸导管插入术对心功能和压力-容积环的双心室评估

通过压力-体积环路分析确定心脏对β肾上腺素能刺激的反应

心脏压力容量环分析小鼠使用电导导管

测量压力容量环中的鼠标

缺氧诱导小鼠肺动脉高压模型中的多次静脉推注给药和侵入性血流动力学评估

使用压力-容积电导导管实时检测阿魏酸对大鼠左心室的影响

心导​​管在小鼠测量压力体积的关系:调查的影响鲍迪奇

摘要

探索更多视频

此视频中的章节

左冠状动脉前降支的小鼠结扎:对心肌梗死后重塑和心衰模型

小鼠急性心肌梗死的实时压力容积分析

小鼠右心室系统及缺氧诱发肺动脉高血压的侵入性血液动力学评估

Quantification of Biventricular Function and Morphology by Cardiac Magnetic Resonance Imaging in Mice with Pulmonary Artery Banding

小鼠闭胸导管插入术对心功能和压力-容积环的双心室评估

通过压力-体积环路分析确定心脏对β肾上腺素能刺激的反应

心脏压力容量环分析小鼠使用电导导管

测量压力容量环中的鼠标

缺氧诱导小鼠肺动脉高压模型中的多次静脉推注给药和侵入性血流动力学评估

使用压力-容积电导导管实时检测阿魏酸对大鼠左心室的影响

心导管在小鼠测量压力体积的关系:调查的影响鲍迪奇