VENTRICULAR SYSTOLIC INTERACTIONS DURING HEART FAILURE

右(RV)与左(LV)功能的相互依赖 脑室是由于共同肌肉在解剖上的紧密联系。 游离壁和共享室间隔中的纤维。虽然 在这项资助中，大多数研究都对舒张期相互作用感兴趣。 我们关注的是心脏收缩时的相互作用，并假设RV 收缩功能在其相当大一部分中依赖于左心室。 收缩力。这种交互对于 RV功能的维持，不仅在正常心脏，而且在 各种疾病状况，如右心衰竭或肺 高血压，以及在使用左心辅助装置期间。我们的 目的是确定单纯性收缩对右室功能的影响 瞬间降低左心室内压，无需 改变右室或左室舒张末压力或容量。的LV尖端 麻醉的猪将连接到一个人造脑室，这是 已计时在舒张期后立即充填。心脏研究将从 用我们的快速心力衰竭模型复制正常猪和心力衰竭后的猪 心脏起搏，我们已经在一个真实的模型中展示了结果 扩张性充血性心力衰竭。每颗心脏都会被植入仪器 用微尖导管测量右室和左室压力， 用肺动脉血流探头检测瞬时心输出量 并用超声晶体测量LV间隔至自由壁的尺寸。数据将 由计算机采样，并将单个卸载的节拍与 在变化的预载荷条件下，在稳态正常搏动之前 和后负荷，带和不带心包。LV到RV的压力 增益(Gplr)和流量增益(Gflr)将计算为瞬时 右室压力和肺流量的变化与LP变化的比率 收缩时压力与时间的函数关系，以及每搏功增加 (Grvsw)将作为RV冲程工作的综合变化来计算 除以积分变化的LV压力时间积分。我们的 初步数据显示了归一化(%/%)的Gplr、Gflr和 在正常心脏中，Grvsw分别为0.136、0.237和0.513，这意味着51% 房车的冲程功的一半是由于LV。来自生猪的初步数据 在心力衰竭方面，这表明收益明显更高 (Grvsw=0.81)。有了这些数据，我们将确认 假设高达20%的右室收缩压来自 在正常心脏中，RV对LVP的依赖性更强。 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.