Hunter W C
Department of Biomedical Engineering, Johns Hopkins Medical School, Baltimore, Maryland 21205.
Circ Res. 1989 Feb;64(2):265-75. doi: 10.1161/01.res.64.2.265.
Ejection has previously been thought to exert only negative effects on end-systolic left ventricular pressure, via mechanisms like shortening deactivation and the force-velocity relation. Whether ejection also exerted a positive influence on pressure generation was tested by comparing two successive beats: 1) the last beat of steady-state ejection versus 2) a totally isovolumic contraction at the end-systolic volume. In 12 isolated, blood-perfused canine hearts loaded with a simulated arterial system, ejecting end-systolic pressure exceeded isovolumic pressure by approximately 10 mm Hg when ejection fraction was 0.3. With both higher and lower ejection fractions, the excess of ejecting end-systolic pressure was smaller; beyond an ejection fraction of roughly 0.5, the trend reversed so that ejecting end-systolic pressure fell below isovolumic pressure. The maximum excess in ejecting end-systolic pressure was quite variable (1-17 mm Hg), but the pattern of its variation with ejection fraction was consistent. A correlate of the positive effect of ejection on ventricular pressure was found in the timing of end systole. For an ejection fraction of 0.4, the systolic duration of ejecting beats was approximately 45% longer than in isovolumic beats (range, 23-67%). Potentially, a positive effect of ejection might be due to a residual influence of the stronger activation of cardiac myofilaments early in ejecting systole during which the sarcomeres were at longer lengths than in the isovolumic beat at end-systolic volume (length-dependent activation). A hypothetical model based on this mechanism reproduced both of the positive effects of ejection that were observed: excess end-systolic pressure and prolonged duration of systole. Thus, the approximate load independence of end-systolic pressure could result from the counter balance between opposing influences of ejection.
以往认为，射血仅通过缩短失活和力-速度关系等机制对收缩末期左心室压力产生负面影响。通过比较两个连续的心搏来测试射血是否也对压力产生有积极影响：1）稳态射血的最后一个心搏与2）收缩末期容积下的完全等容收缩。在12个灌注血液的离体犬心脏中，加载模拟动脉系统，当射血分数为0.3时，射血收缩末期压力比等容压力高约10 mmHg。射血分数较高和较低时，射血收缩末期压力的差值都较小；超过约0.5的射血分数时，趋势逆转，射血收缩末期压力低于等容压力。射血收缩末期压力的最大差值变化很大（1-17 mmHg），但其随射血分数变化的模式是一致的。在收缩末期的时间安排中发现了射血对心室压力产生积极影响的一个相关因素。对于0.4的射血分数，射血心搏的收缩期持续时间比等容心搏长约45%（范围为23-67%）。射血的积极作用可能是由于射血收缩早期心肌肌丝更强激活的残余影响，在此期间肌节长度比收缩末期容积下等容心搏时更长（长度依赖性激活）。基于该机制的一个假设模型再现了观察到的射血的两个积极作用：收缩末期压力过高和收缩期持续时间延长。因此，收缩末期压力近似的负荷独立性可能是射血相反影响之间平衡的结果。
