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(Circulation. 1996;94:1475-1482.)
© 1996 American Heart Association, Inc.

Articles

Rapid Shortening During Relaxation Increases Activation and Improves Systolic Performance

Matthew W. Watkins, MD; Akihiro Higashiyama, MD; Zengyi Chen, MD; Martin M. LeWinter, MD

the Cardiology Unit, The University of Vermont, Burlington.

Background 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.

Methods and Results 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 E_max (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 (O₂) 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 O₂ (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.

Conclusions 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 O₂ associated with ejection suggests a positive interaction between myofilament shortening and activator calcium cycling.

Key Words: calcium • contractility • mechanics • sarcoplasmic reticulum

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