Aghajani Ebrahim, Muller Stig, Kjørstad Knut E, Korvald Christian, Nordhaug Dag, Revhaugand Arthur, Myrmel Truls
Department of Surgery, Institute of Clinical Medicine, University of Tromsø, N-9038 Tromsø, Norway.
Shock. 2006 Apr;25(4):370-6. doi: 10.1097/01.shk.0000209521.20496.7a.
Our previous studies indicate that left ventricular end-systolic pressure-volume relations (ESPVRs) or elastance (Ees) are not reduced in studies where expected reductions of contractility should be found (i.e., heart failure, stunning, and endotoxemia). The present study was done to assess whether this phenomenon is due to a particular load sensitivity of elastance, rendering this index inappropriate as a measurement of contractility in pathologic states in vivo.
Analysis of previously generated data revealed an increased ESPVR in stunned hearts, in pigs made endotoxemic, and in hearts rapidly paced. After inducing acute heart failure by microembolization, the ESPVR was increased when assessed using linear relations but reduced when assessing ESPVR by a curvilinear algorithm. To further evaluate the effect of different load alterations on ESPVR, this relation was generated by (i) inferior vena caval occlusions (VCOs); (ii) gradually occluding the descending aorta (pressure interventions); and (iii) rapidly infusing blood (120 mL) into the left atrium (volume increments). The load protocol was applied in 5 pigs, before and after the left ventricle was stunned by 11 brief left main coronary artery occlusions/reperfusions (accumulated ischemia 20 min affecting 81% of the left ventricle). Correlation coefficients for left ventricular elastance ranged from 0.93 to 0.99 in all the 3 types of loading interventions. Despite significant reductions in stroke volume, stroke work, and dP/dtmax, VCO-calculated linear and curvilinear Ees increased 90 min after stunning (55% +/- 4% and 94% +/- 6%, respectively). Linear Ees during pressure interventions decreased 36% +/- 1%, whereas curvilinear Ees decreased 33% +/- 3%. During volume infusions, linear Ees decreased 27% +/- 2%. We achieved the same results after blocking the baroreceptor reflexes using hexamethonium.
The Ees is particularly load dependent and will reflect load interventions more than the inotropic state of the cardiac muscle. A VCO-generated Ees increase could be an unmasking of a pronounced preload sensitivity in failing myocardium.
我们之前的研究表明，在预期应发现收缩性降低的研究中（即心力衰竭、心肌顿抑和内毒素血症），左心室收缩末期压力-容积关系（ESPVRs）或弹性（Ees）并未降低。本研究旨在评估这种现象是否是由于弹性的特定负荷敏感性所致，从而使该指标不适用于体内病理状态下收缩性的测量。
对先前生成的数据进行分析发现，在心肌顿抑的心脏、内毒素血症猪以及快速起搏的心脏中，ESPVR增加。通过微栓塞诱导急性心力衰竭后，使用线性关系评估时ESPVR增加，而通过曲线算法评估ESPVR时则降低。为了进一步评估不同负荷改变对ESPVR的影响，通过以下方式生成这种关系：（i）下腔静脉阻塞（VCO）；（ii）逐渐阻塞降主动脉（压力干预）；（iii）快速向左心房输注血液（120 mL）（容量增加）。在5头猪身上应用负荷方案，在左心室通过11次短暂的左主冠状动脉阻塞/再灌注（累积缺血20分钟，累及81%的左心室）造成心肌顿抑之前和之后。在所有3种负荷干预类型中，左心室弹性的相关系数范围为0.93至0.99。尽管每搏量、每搏功和dP/dtmax显著降低，但VCO计算的线性和曲线Ees在心肌顿抑后90分钟增加（分别为55%±4%和94%±6%）。压力干预期间的线性Ees降低36%±1%，而曲线Ees降低33%±3%。在容量输注期间，线性Ees降低27%±2%。使用六甲铵阻断压力感受器反射后，我们得到了相同的结果。
Ees特别依赖负荷，并且将更多地反映负荷干预而非心肌的变力状态。VCO产生的Ees增加可能是衰竭心肌中明显的前负荷敏感性的一种揭示。
