Effect of Calcium on Force-Velocity-Length Relations of Heart Muscle of the Cat

Brutsaert, Dirk L.; Claes, Victor; Goethals, M A

doi:10.1161/01.res.32.3.385

Cited by 67 publications

(38 citation statements)

References 28 publications

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“…After the elastic damping of the force-lengthvelocity lever feedback system was adjusted to compensate for electromechanical transients, the maximum velocity of unloaded muscle shortening (Vm.,) was obtained by abruptly decreasing the load on the muscle at the time of activation (zero load clamp). 33 The output of the amplifier of the Gould 2400 s recorder was connected to an electronic differentiator, and both of these were fed into an analog-to-digital converter (model DT 2821-F-801, Data Translation Inc., Marlborough, Mass. ), which in turn was connected to a microcomputer (model 286, COMPAQ Computer Corp., Houston, Tex.).…”

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confidence: 99%

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Rouleau

Andries

et al. 1993

Circulation Research

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Vascular endothelium has been shown to modify the contractile characteristics of vascular smooth muscle, and endocardial endothelium has been shown to modify the contractile characteristics of adjacent myocardium. In this study, whether vascular endothelium also modifies the contractile characteristics of adjacent myocardium and whether these effects are additive to those of endocardial endothelium were investigated. Rabbit hearts (n=54) were excised and mounted in a Langendorif preparation. Vascular reactivity was verified by acetylcholine infusion. One group of these hearts had Triton X-100 injected as a bolus into the coronaries to render the vascular endothelium dysfunctional. The other portion served as control hearts. Triton X-100 bolus injection resulted in little or no pathological changes on morphological examination; however, the vasodilatory response to acetylcholine in these hearts was abolished, suggesting vascular endothelial dysfunction. Vascular smooth muscle reactivity was verified in Triton X-100-injected hearts by nitroprusside infusion. In the control Langendorff-perfused hearts, there was little evidence of vascular endothelial dysfunction, with the coronary perfusion rate increasing from 8.9±0.4 to 11.0±0.3 ml/g per minute (p<0.01) in response to acetylcholine. All hearts were then removed, and right ventricular papillary muscles were excised for myocardial mechanical studies. Control Langendorffperfused hearts had myocardial mechanical characteristics similar to those of muscles from 18 other control hearts without Langendorff perfusion, indicating that the Langendorff perfusion itself had little effect on myocardial mechanics. The muscles from the Triton X-100-injected Langendorff hearts had marked changes: a shortening of twitch duration (363± 16 versus 449±9 msec, p<0.01) and decreases in total tension (2.2±0.2 versus 2.9±0.2 g/mm2, p<0.01), dT/dt (9±1 versus 12±1 g/mm2 per second, p<0.05), and maximum velocity of unloaded muscle shortening (Vmax) (0.89±0.06 versus 1.14±0.07 length at which maximum developed tension occurred [Lm.]/sec, p<0.05). Endocardial endothelial removal of the papillary muscles in the two control groups (with and without Langendorif perfusion) by Triton X-100 caused the same changes in twitch characteristics as occurred in muscles from the Langendorff-perfused hearts injected with Triton X-100 but with intact endocardial endothelium, suggesting that vascular endothelial dysfunction had similar effects on contractile characteristics as endocardial endothelial removal. Endocardial endothelial removal of the papillary muscles from Langendorif-perfused hearts that had a bolus injection of Triton X-100 caused further shortening of twitch duration and a further decrease in total tension (1.7±0.2 versus 2.1±0.1 g/mm2, p

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confidence: 99%

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Rouleau

Andries

et al. 1993

Circulation Research

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“…18,22,23 In those experiments, activation was varied in one of several ways, including inotropic agents such as ␤-agonists, increased [Ca 2ϩ ] o , or measuring loaded shortening at various times during twitch contractions. Despite the consistent finding of Ca 2ϩ -induced alterations in power output, the subcellular factors that limit loaded shortening and relative power output in cardiac muscle remained uncertain.…”

Section: Discussionmentioning

confidence: 99%

Strongly Binding Myosin Crossbridges Regulate Loaded Shortening and Power Output in Cardiac Myocytes

McDonald

Moss

2000

Circulation Research

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Abstract-This study investigated the possible roles of strongly binding myosin crossbridges in determining loaded shortening and power output in cardiac myocytes. Single skinned cardiac myocytes were attached between a force transducer and position motor, and shortening velocities were measured over a range of loads during varying levels of Ca 2ϩ activation. Lowering the [Ca 2ϩ ] slowed shortening velocities, decreased relative power output, and increased the curvature of length traces. We tested the hypothesis that Ca 2ϩ activation dependence of loaded shortening is determined primarily by strongly binding crossbridges or by [Ca 2ϩ ] per se, which was done by measuring loaded shortening before and after addition of N-ethylmaleimide-conjugated myosin subfragment-1 (NEM-S1), a strongly binding myosin analogue that cooperatively enhances thin filament activation. At fixed [Ca 2ϩ ], NEM-S1 reduced the curvature of length traces and sped loaded shortening velocities. Even when [Ca 2ϩ ] was adjusted so that force was equal with and without NEM-S1, myocyte shortening was faster and exhibited less curvature with NEM-S1. In the presence of NEM-S1, peak relative power output was also significantly greater during activations either at the same [Ca 2ϩ ] or when [Ca 2ϩ ] was adjusted to achieve the same force. Consequently, NEM-S1 eliminated any Ca 2ϩ dependence of relative power output that is normally observed in cardiac myocytes. These results indicate that strongly binding crossbridges play a significant role in determining loaded shortening and power output and suggest that previously observed Ca Key Words: cardiac myocytes Ⅲ power output Ⅲ myosin M yocardium shortens against an afterload as blood is expelled into the circulation during systole. The amount of blood expelled is ultimately determined by the rate of myocardial shortening, which depends on several factors and varies inversely with afterload. Considerable information regarding the relationship between stroke volume and afterload has been obtained by characterizing force-velocity relationships in isolated, multicellular preparations of myocardium. Although these experiments have enriched our understanding of myocardial contraction, the presence of extracellular elasticity has confounded the interpretation of these relationships and made it difficult to assess how afterload influences the contractile machinery. The recent development of single skinned myocyte preparations for dynamic mechanical measurements circumvents several of the complexities associated with intercellular elasticity in multicellular preparations and has added to our understanding of myofibrillar behavior during loaded shortening. In single skinned myocyte preparations, as with multicellular preparations, force-velocity relationships are hyperbolic and are highly sensitive to changes in myoplasmic [Ca 2ϩ ]. 1,2 Also, the time course of loaded shortening changes when Ca 2ϩ activation levels are reduced in skinned myocyte preparations. Lowering the [Ca 2ϩ ] not only yields sl...

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“…Brustsaert et al (1973) have reported an increase in V'max following an increase in Ca++ concentration in the bathing medium and suggested that changes in Ca++ concentration influence the rate of turnover of cross-bridge formation between actin and myosin. The present study indicates that thiamylal and halothane may depress the Ca-regulated turnover rate of cross-bridge formation, but the depression of turnover rate by halothane is not completely counteracted by increasing Ca++ concentration.…”

Section: Discussionmentioning

confidence: 99%

Effects of change in concentration of calcium on myocardial contractility depressed by thiamylal and halothane.

Iwatsuki

1976

Tohoku J. Exp. Med.

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Effect of Calcium on Force-Velocity-Length Relations of Heart Muscle of the Cat

Cited by 67 publications

References 28 publications

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Effect of dysfunctional vascular endothelium on myocardial performance in isolated papillary muscles.

Strongly Binding Myosin Crossbridges Regulate Loaded Shortening and Power Output in Cardiac Myocytes

Effects of change in concentration of calcium on myocardial contractility depressed by thiamylal and halothane.

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