VENTRICULAR SYSTOLIC INTERACTIONS DURING HEART FAILURE

右（RV）和左（LV）之间的功能相互依赖性 心室是由于共同肌肉的紧密解剖连接 游离壁和共用室间隔中的纤维。 虽然 大多数研究都对舒张期的相互作用感兴趣， 我们关注收缩期的相互作用，并假设RV 心脏收缩功能在很大程度上依赖于左心室， 收缩力 这种相互作用对于 维持RV功能，不仅在正常心脏中， 各种疾病状况如右心衰竭或肺 高血压，以及在使用左心室辅助装置期间。 我们 目的是确定单独收缩对RV功能的影响， 在单次心跳中立即降低左心室压力， 改变RV或LV舒张末期压或容积。 左心室心尖部 麻醉的猪将连接到人工心室， 定时填充后立即关闭。 心脏将被研究， 正常猪和心力衰竭后，与我们的快速模型， 心室起搏，我们已经在一个真实的模型中显示了结果， 扩张性充血性心力衰竭 每颗心脏都将被植入 使用微尖端导管测量RV和LV腔室压力， 用肺动脉流量探头测量的瞬时RV心输出量，以及RV 和超声晶体的左心室间隔至游离壁尺寸。 数据将 将被计算机采样，并且将单个未加载的搏动与 在变化的前负荷条件下，之前的稳态正常搏动 和后负荷，以及有无心包。 LV至RV压力 增益（Gplr）和流量增益（Gflr）将被计算为瞬时 RV压力和肺血流变化与LP变化的比值 收缩期压力与时间的函数关系，以及每搏功增益 （Grvsw）将计算为RV冲程功的综合变化 除以LV压力时间积分的积分变化。 我们 初步数据表明Gplr、Gflr和Gflr的标准化（%/%）值， 正常心脏的Grvsw分别为0.136，0.237和0.513，这意味着51%的 右心室的冲程功的90%是由左心室引起的。 猪的初步数据 在心力衰竭中， （Grvsw=0.81）。 有了这些数据，我们将确认 假设高达20%的RV收缩压是从 在正常心脏中，RV更依赖于LVP， 充血性心力衰竭

The interdependence of function between the right (RV) and left (LV) ventricles is due to the close anatomical connections of the common muscle fibers in the free walls and the shared interventricular septum. Although most studies have been interested in diastolic interactions, in this grant we are concentrating on systolic interactions and hypothesize that RV systolic function is dependent on the LV for a sizeable fraction of its contractile force. This interaction can be quite important to the maintenance of RV function, not only in the normal heart, but during various disease conditions such as right heart failure or pulmonary hypertension, and during the use of left ventricular assist devices. Our goal is to determine the isolated systolic effects on RV function of instantaneously reducing left ventricular pressure in a single beat without changing RV or LV end-diastolic pressure or volume. The LV apex of anesthetized pigs will be connected to a prosthetic ventricle which is timed to fill immediately after diastole. Hearts will be studied from normal pigs and after heart failure is produced with our model of rapid ventricular pacing, which we have shown results in a realistic model of dilated congestive heart failure. Each heart will be instrumented for measurements of RV and LV chamber pressures with microtip catheters, instantaneous RV cardiac output with a pulmonary artery flow probe, and RV and LV septal-to-free wall dimensions with ultrasonic crystals. Data will be computer-sampled and a single unloaded beat will be compared to the preceeding steady-state normal beats, under conditions of varying preload and afterload, and with and without the pericardium. The LV to RV pressure gain (Gplr) and flow gain (Gflr) will be calculated as the instantaneous ratios of changes in RV pressure and pulmonary flow to change in LP pressure as a function of time during systole, and the stroke work gain (Grvsw) will be calculated as the integrated change in RV stroke work divided by integrated changes in LV pressure time integral. Our preliminary data demonstrate normalized (%/%) values of Gplr, Gflr, and Grvsw of 0.136, 0.237, and 0.513 in the normal heart, which means that 51% of the stroke work of the RV is due to the LV. Preliminary data from pigs in heart failure suggest that the gains are significantly higher (Grvsw=0.81) than in normal hearts. With these data we will confirm the hypothesis that up to 20% of RV systolic pressure is transmitted from the LV in the normal heart, and that the RV is even more dependent on LVP in congestive heart failure.