Rapid shortening during relaxation increases activation and improves systolic performance.
Rapid shortening during relaxation increases activation and improves systolic performance.
复制标题
放松期间的快速缩短增加了激活并改善了收缩性能。
DOI：
10.1161/01.cir.94.6.1475
复制
发表时间：
1996
期刊：
影响因子：
37.8
通讯作者：
LeWinter,MM
中科院分区：
文献类型：
--
作者：
Watkins,MW;Higashiyama,A;Chen,Z;LeWinter,MM
背景先前对心肌和离体心制剂的研究一般将射血的积极作用归因于更大的长度依赖的激活。然而，已经有一些报告表明，与舒张期末容量(EDV)史无关的射血相关的收缩功能增加。本研究旨在更全面地表征后一种效应在完整心室中的机械能结果。方法和结果在收缩末期使用伺服运动启动左心室容积减少(VR)，同时保持EDV恒定。在等容收缩、慢收缩(5.0±0.9EDV/S)和快收缩(2 6.8±5.1 EDV/S)三种状态下，对7只红细胞灌流的兔心进行了恒定EDV的研究。与等容搏动相比，VR使心脏的收缩能力增强。快速虚拟现实的这种影响更大，需要50次拍子才能达到稳定状态。快速VR使发展压增加15%(平均±23.7比105.9±27.6 mm Hg)，最大dp/dt增加17%(1223±401比1435±505 mm Hg·S−1)，Emax(收缩末压-容量关系斜率)增加13%(69.4±19.9比78.6±23.0 mm 汞/毫升)(均P<0.01)。左心室耗氧量(V̇O2)慢速时无明显变化，快速时降低8%(0.0744±0.0194对0.0683±0.0141 mLO2·Beat−1·100g−1；P<；0.05)。在独立心脏(n=8)中，使用2，3-丁二酮单肟估计成本(基础代谢和兴奋-收缩偶联)。与对照组相比，快速VR组非机械性V-̇O2增加26%(0.0248±0.0021对0.0312±0.0022 mLO2·Beat−1·100g−1；P<；01)，与每搏动循环的钙离子增加一致。结论收缩末期后射血对心室功能有积极的影响，但不能归因于长度依赖的激活，这可能与可供激活的钙增加有关。同样，与射血相关的非机械性V-̇O2的增加表明肌丝缩短和激活剂钙循环之间存在积极的相互作用。
BackgroundPrevious 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.Methods and ResultsA 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) (allP<.01). Left ventricular oxygen consumption (V̇o2) 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 V̇o2(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.ConclusionsEjection 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 V̇o2associated with ejection suggests a positive interaction between myofilament shortening and activator calcium cycling.