Santamore W P, Li K S, Nakamoto T, Johnston W E
Philadelphia Heart Institute, Presbyterian Medical Center, PA 19104.
Cardiovasc Res. 1990 Sep;24(9):768-76. doi: 10.1093/cvr/24.9.768.
The mechanical coupling between the ventricles occurs directly through the myocardium (ventricular-ventricular coupling) and indirectly through the pericardium (ventricular-pericardial-ventricular coupling). We postulated that the magnitude of ventricular-pericardial-ventricular coupling would increase at high pericardial pressures, while ventricular-ventricular coupling would be unaltered.
Canine hearts were removed and placed in cold cardioplegic solution. Balloons were inserted into each ventricle and the left and right ventricular pressure (dP1, dPr) and volume (dV1, dVr) changes caused by increasing the pressure and volume of the other ventricle and by increasing pericardial pressure (dPp) were measured.
Hearts from 10 random source dogs, weight 12.5-18 kg, were used.
At control pericardial pressure levels, the magnitude of the pericardial-ventricular interactions was greater than the ventricular-ventricular interactions: dP1/dPp was significantly greater than dP1/dPr, at 0.71 (SEM 0.04), n = 6, v 0.18 (0.03), p less than 0.01, and dV1/dPp was significantly greater than dV1/dPr, at -0.83 (0.09) v -0.24 (0.06), p less than 0.05. Raising the pericardial pressure increased the mechanical coupling between the ventricles: dP1/dPr approximately, dV1/dPr approximately, dPr/dP1 approximately, and dVr/dP1 approximately increased significantly (p less than 0.05) by 0.48 (0.03), 0.67 (0.13), 0.38 (0.05), and 0.61 (0.09) respectively. This increased coupling occurred through pericardial pressure changes. If pericardial pressure was maintained constant, the coupling between the ventricles was unaltered. This same pattern was observed in four in situ experiments. For these experiments, at the raised pericardial pressure levels, dP1/dPr increased, from 0.51 (0.03) to 0.79 (0.01), p less than 0.05, if pericardial pressure was allowed to vary, but was unaltered with a constant pericardial pressure, at 0.42 (0.03) v 0.44 (0.04), p greater than 0.5.
Ventricular interdependence was increased with raised pericardial pressure and this increased coupling was due primarily to an increased ventricular-pericardial-ventricular coupling. This increased coupling may help to explain the paradoxical pulse observed in cardiac tamponade.
心室之间的机械耦联直接通过心肌发生（心室 - 心室耦联），并间接通过心包发生（心室 - 心包 - 心室耦联）。我们推测，在心包压力升高时，心室 - 心包 - 心室耦联的程度会增加，而心室 - 心室耦联则保持不变。
取出犬心并置于冷心脏停搏液中。将球囊插入每个心室，测量另一心室压力和容积增加以及心包压力（dPp）增加时左、右心室压力（dP1、dPr）和容积（dV1、dVr）的变化。
使用来自10只随机来源犬的心脏，体重12.5 - 18千克。
在心包压力处于对照水平时，心包 - 心室相互作用的程度大于心室 - 心室相互作用：dP1/dPp显著大于dP1/dPr，分别为0.71（标准误0.04），n = 6，对比0.18（0.03），p < 0.01；dV1/dPp显著大于dV1/dPr，分别为 - 0.83（0.09）对比 - 0.24（0.06），p < 0.05。升高心包压力会增加心室之间的机械耦联：dP1/dPr、dV1/dPr、dPr/dP1和dVr/dP1分别显著增加（p < 0.05），增加幅度分别为0.48（0.03）、0.67（0.13）、0.38（0.05）和0.61（0.09）。这种耦联增加是通过心包压力变化实现的。如果心包压力保持恒定，心室之间的耦联则不变。在四个原位实验中观察到了相同的模式。对于这些实验，在升高的心包压力水平下，如果允许心包压力变化，dP1/dPr从0.51（0.03）增加到0.79（0.01），p < 0.05；但在心包压力恒定时则不变，分别为0.42（0.03）对比0.44（0.04），p > 0.5。
心包压力升高会增加心室相互依赖性，这种耦联增加主要是由于心室 - 心包 - 心室耦联增加。这种增加的耦联可能有助于解释心脏压塞时出现的奇脉。
