Watkins M W, Higashiyama A, Chen Z, LeWinter M M
Cardiology Unit, University of Vermont, Burlington 05401, USA.
Circulation. 1996 Sep 15;94(6):1475-82. doi: 10.1161/01.cir.94.6.1475.
Previous studies in cardiac muscle and isolated heart preparations generally have attributed positive effects of ejection to greater length-dependent activation. However, there have been some reports of an ejection-related increase in contractile function that is independent of end-diastolic volume (EDV) history. The present study was designed to more fully characterize the mechanoenergetic results of the latter effect in the intact ventricle.
A servomotor was used to initiate left ventricular volume reduction (VR) at end systole, with EDV kept constant. Seven isolated, red blood cell-perfused rabbit hearts were studied at constant EDV during isovolumic contraction, slow VR (5.0 +/- 0.9 EDV/s), and rapid VR (26.8 +/- 5.1 EDV/s). Compared with isovolumic beats, VR caused an enhancement in contractility. This effect was greater for rapid VR and required > 50 beats to attain steady state. Rapid VR increased developed pressure by 15% (92.2 +/- 23.7 [mean +/- SD] versus 105.9 +/- 27.6 mm Hg), maximum dP/dt by 17% (1223 +/- 401 versus 1435 +/- 505 mm Hg.s-1), and Emax (slope of the end-systolic pressure-volume relation) by 13% (69.4 +/- 19.9 versus 78.6 +/- 23.0 mm Hg/mL) (all P < .01). Left ventricular oxygen consumption (VO2) was unchanged with slow VR and decreased by 8% with rapid VR (0.0744 +/- 0.0194 versus 0.0683 +/- 0.0141 mL O2.beat-1.100 g-1; P < .05). In separate hearts (n = 8), costs (basal metabolism and excitation-contraction coupling) were estimated by use of 2,3-butanedione monoxime. Compared with control, rapid VR was associated with a 26% increase in nonmechanical VO2 (0.0248 +/- 0.0021 versus 0.0312 +/- 0.0022 mL O2.beat-1.100 g-1; P < .01), consistent with an increase in calcium cycled per beat.
Ejection after end systole has a positive effect on ventricular performance that cannot be ascribed to length-dependent activation and is likely related to an increase in calcium available for activation. Similarly, an increase in nonmechanical VO2 associated with ejection suggests a positive interaction between myofilament shortening and activator calcium cycling.
先前在心肌和离体心脏标本中的研究通常将射血的积极作用归因于更大程度的长度依赖性激活。然而，有一些报告称，收缩功能的射血相关增加与舒张末期容积（EDV）历史无关。本研究旨在更全面地描述完整心室中后一种效应的机械能量学结果。
使用伺服电机在收缩末期启动左心室容积减少（VR），同时保持EDV恒定。在等容收缩、缓慢VR（5.0±0.9 EDV/s）和快速VR（26.8±5.1 EDV/s）期间，对7个离体的、红细胞灌注的兔心脏在恒定EDV下进行研究。与等容搏动相比，VR导致收缩力增强。这种效应在快速VR时更大，并且需要超过50次搏动才能达到稳态。快速VR使舒张末期压力增加15%（92.2±23.7[平均值±标准差]对105.9±27.6 mmHg），最大dP/dt增加17%（1223±401对1435±505 mmHg·s-1），Emax（收缩末期压力-容积关系的斜率）增加13%（69.4±19.9对78.6±23.0 mmHg/mL）（所有P<.01）。左心室氧耗（VO2）在缓慢VR时不变，在快速VR时下降8%（0.0744±0.0194对0.0683±0.0141 mL O2·搏动-1·100 g-1；P<.05）。在另外的心脏（n = 8）中，使用2,3-丁二酮单肟估计能量消耗（基础代谢和兴奋-收缩偶联）。与对照组相比，快速VR与非机械性VO2增加26%相关（0.0248±0.0021对0.0312±0.0022 mL O2·搏动-1·100 g-1；P<.01），这与每搏钙循环增加一致。
收缩末期后的射血对心室功能有积极作用，这不能归因于长度依赖性激活，并且可能与可用于激活的钙增加有关。同样，与射血相关的非机械性VO2增加表明肌丝缩短与激活钙循环之间存在积极相互作用。
