Sugiura S, Hunter W C, Sagawa K
Department of Biomedical Engineering, Johns Hopkins Medical School, Baltimore, Maryland 21205.
Circ Res. 1989 Feb;64(2):255-64. doi: 10.1161/01.res.64.2.255.
We studied the effect of ejection on end-systolic pressure in isolated heart preparations. Ejecting beats were compared with isovolumic beats having the same volume as at end systole. While holding end-systolic volume constant, various stroke volumes, including negative stroke volumes (volume injected during systole), were imposed using a predetermined volume command. After switching contraction mode between ejecting and isovolumic, we measured the immediate and steady changes in end-systolic pressure. In the first isovolumic beat after switching from steady-state ejecting beats, the change in end-systolic pressure was variable, depending on the stroke volume. The end-systolic pressure of the ejecting beat exceeded that of the isovolumic beat on average by up to 18 mm Hg with small stroke volume, but the ejecting end-systolic pressure became lower than isovolumic with either large stroke volume (stroke volume/end-systolic volume less than 0.96) or with negative stroke volume. During the transient phase following a switch from ejecting to isovolumic, the end-systolic pressure gradually decreased to a steady state. Consequently, even in steady state, ejecting end-systolic pressure exceeded isovolumic pressure over a significant range of stroke volume (stroke volume/end-systolic volume less than 1.18). After returning contraction mode from isovolumic back to ejecting, we observed responses that were a mirror image. These results indicated that in addition to negative uncoupling effect, ejection exerts positive effects on ventricular end-systolic pressure that are manifest both quickly and gradually. We hypothesized that the mechanism responsible for the positive effect is length-dependent activation via the larger volume (both at the initiation of contraction and averaged over a cardiac cycle) of a beat that ejects compared to one held isovolumic at end-systolic volume. The results with volume injection were consonant with this concept.
我们研究了射血对离体心脏标本中收缩末期压力的影响。将射血搏动与收缩末期容积相同的等容搏动进行比较。在保持收缩末期容积恒定的情况下，使用预定的容积指令施加各种搏出量，包括负搏出量（收缩期注入的容积）。在将收缩模式在射血和等容之间切换后，我们测量了收缩末期压力的即时和稳定变化。在从稳态射血搏动切换后的第一个等容搏动中，收缩末期压力的变化是可变的，取决于搏出量。小搏出量时，射血搏动的收缩末期压力平均比等容搏动高出多达18 mmHg，但大搏出量（搏出量/收缩末期容积小于0.96）或负搏出量时，射血收缩末期压力低于等容压力。在从射血切换到等容后的过渡阶段，收缩末期压力逐渐降至稳态。因此，即使在稳态下，在相当大的搏出量范围内（搏出量/收缩末期容积小于1.18），射血收缩末期压力也超过等容压力。在将收缩模式从等容恢复到射血后，我们观察到了镜像反应。这些结果表明，除了负解耦效应外，射血对心室收缩末期压力有积极影响，这种影响既有快速的也有逐渐的表现。我们假设，产生这种积极影响的机制是通过与在收缩末期容积保持等容的搏动相比，射血搏动更大的容积（在收缩开始时以及整个心动周期的平均值）实现的长度依赖性激活。容积注入的结果与这一概念相符。
