Active Shortening Retards the Decline of the Intracellular Calcium Transient in Mammalian Heart Muscle

Housmans, Philippe R.; Lee, Norman K M.; Blinks, John R.

doi:10.1126/science.6857274

Cited by 175 publications

(87 citation statements)

References 24 publications

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“…24 Because of the higher sensitivity of myofilament for calcium, the time course of relaxation is determined by calcium unbinding from troponin C rather than by calcium sequestration by the sarcoplasmic reticulum. 25 ] o is decreased, is consistent with the fact that calcium per se modulates myofilament calcium sensitivity, according to the cooperativity concept. 26,27 At the end of the study, the muscle cross-sectional area was calculated from the length and weight of papillary muscle, assuming a density of 1.…”

Section: Mechanical Parameterssupporting

confidence: 66%

Effects of bupivacaine, levobupivacaine and ropivacaine on myocardial relaxation

David

Ferreti

Amour

et al. 2007

Can J Anesth/J Can Anesth

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CAN J ANESTH 54: 3 www.cja-jca.org March, 2007 Purpose: Ropivacaine and levobupivacaine were developed to reduce the risk of occasional toxicity reported with bupivacaine. While the effects of long-acting local anesthetics (LAAs) on myocardial contractility (inotropy) are well described, their effects on relaxation (lusitropy) remain largely unknown. The present study aimed to compare the effects of LAAs on rat myocardium. Methods:Left ventricular papillary muscles of male Wistar rats were used to compare the inotropic and lusitropic responses of increasing concentrations of LAAs (10 -8 to 10 -3 M) under isometric and isotonic conditions. Data are mean % (SD) of baseline value.Results: Long-acting local anesthetics induced a significant impairment of relaxation in isotonic and isometric conditions. As compared to ropivacaine, bupivacaine and levobupivacaine induced greater negative lusitropic effects in isotony [at 10 -3 M, maximum unloaded shortening velocity ( max Vr) = 27 ± 11 vs 13 ± 6 and 8 ± 5%] and isometry (at 10 -3 M, time-to-halfrelaxation: 106 ± 10 vs 127 ± 17 and 133 ± 17%). When the comparison was made with equipotent concentrations, the negative lusitropic effects induced with levobupivacaine were significantly greater than those of bupivacaine and ropivacaine in isometric and isotonic conditions (at 10 -3 M, max Vr = 7 ± 4 vs 13 ± 6 and 17 ± 4 %). As previously described, LAAs also induced concentration-dependent negative inotropic effects that were greater for levobupivacaine compared to equivalent or equipotent concentrations of bupivacaine and ropivacaine.Conclusions: Long-acting local anesthetics induce marked negative inotropic and lusitropic effects. Among LAAs, levobupivacaine exerts the greater depressant effects. Impairment of calcium handling and sarcoplasmic reticulum could explain the differential responses to local anesthetics. Objectif : La ropivacaïne et la lévobupivacaïne ont été dévelop-pées pour réduire le risque d'accidents sévères observés avec la bupivacaïne. Si les effets des anesthésiques locaux (LAAs) sur la contractilité myocardique (inotropie) sont bien décrits, les effets sur la relaxation (lusitropie) restent peu explorés. Cette étude a eu pour objectif de comparer les effets des LAAs chez le rat. Méthode : Les effets de concentrations croissantes de LAAs (10 -8 à 10 -3 M) sur les réponses inotropes et lusitropes ont été comparés à l'aide d'un modèle de muscles papillaires. Les valeurs sont exprimées en % de la valeur de base (moyenne ± ET). Résultats

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Section: Mechanical Parameterssupporting

confidence: 66%

Effects of bupivacaine, levobupivacaine and ropivacaine on myocardial relaxation

David

Ferreti

Amour

et al. 2007

Can J Anesth/J Can Anesth

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“…Since no change in AL was observed when the muscle was in the resting state in normal Tyrode solution (Fig. 2) or when the active tension was suppressed by the administration of BDM (Fig. 7), the increase in AL may be due to the decrease in active tension associated with the release rather than the decrease in muscle length per se, which is thought to decrease the Ca2+ affinity of troponin C (Allen & Kurihara, 1982;Housmans et al 1983;Stephenson & Wendt, 1984;Allen & Kentish, 1985;Cooper, 1990). On the hypothesis outlined above, it can be explained that the initial large decrease in tension produced a quite small increase in AL, whereas the subsequent small oscillatory changes in tension produced a large change in AL, since most of the decrease in initial tension is thought to be due to the reduction in passive tension associated with the length release (Allen & Kentish, 1988).…”

Section: Discussionmentioning

confidence: 99%

“…extra Ca2+) after a quick release in length. Housmans, Lee & Blinks (1983) reported a higher [Ca2+]i during active shortening of cat papillary muscles than during isometric twitches. These observations were attributed to a decrease in the affinity of troponin C for Ca2+ resulting from a decrease in muscle length and/or active tension development, since the extra Ca2+ can be explained by the release of Ca2+ from troponin C into the myoplasm.…”

Section: Introductionmentioning

confidence: 99%

Alterations in intracellular calcium and tension of activated ferret papillary muscle in response to step length changes.

Saeki

Kurihara

Hongo

et al. 1993

The Journal of Physiology

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SUMMARY1. To study the effects of mechanical constraints on the calcium (Ca2") affinity of cardiac troponin C, we analysed the tension and aequorin light (AL, intracellular Ca2") transients in response to a step length change in aequorin-injected ferret right ventricular papillary muscles. The muscle preparations were continuously activated with ouabain (10-4 M) (ouabain contracture) or with high frequency stimuli in the presence of ryanodine (5 jM) (tetanic contraction).2. The tension transient in response to either the release or stretch was oscillatory: tension decreased rapidly during the release and then increased, after which it lapsed into a new steady level in a series of damped oscillations. The opposite was true for the stretch. The oscillatory responses were conspicuous and less damped in ouabainactivated preparations (oscillation frequency of 2-2-2-3 Hz at 22°C and 4-5-4-6 Hz at 30°C) and much more damped in ryanodine-treated preparations.3. The transient AL response was also oscillatory, the time course of which corresponded to that of the transient tension response. Regardless of the difference in the time course of the transients in two different preparations and at two different temperatures, the increase in AL corresponded to the decrease in tension, likewise the decrease in AL to the increase in tension.4. The mean level of AL after release was lower than the control level present just prior to the release in ouabain-activated preparations, but the AL after release finally returned to the nearly control level in ryanodine-treated preparations.5. When the ryanodine-treated muscle was further treated with 2,3-butanedione monoxime (BDM) (20 mM), the tetanic tension decreased remarkably without affecting the AL signal. The tension transient of this preparation was quite similar to that of the resting muscle, which changed in a nearly stepwise fashion; AL was hardly affected by step length changes, as in the resting muscle, in spite of the higher AL level.6. These results suggest that the Ca2+ affinity of cardiac troponin C is increased with an increase in tension (i.e. the cross-bridge attachment) and decreased with a MS 1213 Y. SAEKI, S. KURIHARA, K. HONGO AND E. TANAKA decrease in tension i.e. the cross-bridge detachment), and that the mean [Ca2+]i is lowered by release, at least in a Ca2+-overloaded condition, mainly through the sarcoplasmic reticulum.

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“…The "dissociation" between preloaddependent changes in mechanics and calcium handling has been observed in numerous studies carried out on mammalian and human myocardium [11,12,21,24,[32][33][34][35]. It has been shown in cat [18], rat [16,17,19], mouse [9] and rabbit [20,21] that muscle stretch is not accompanied by increase of Ca 2+ transient amplitude immediately after the stretch but does produce a slow increase.…”

Section: Effect Of Preload On Peak Active Tension and Fluorescencementioning

confidence: 94%

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

Lookin

Protsenko

2011

Open Life Sciences

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Preload-induced changes of active tension and [Ca2+]i are “dissociated” in mammalian myocardium. This study aimed to describe the distinct effects of preload at low and physiological [Ca2+]o. Rat RV papillary muscles were studied in isometric conditions at 25‡C and 0.33 Hz at 1 mM (hypo-Ca group) and 2.5 mM [Ca2+]o (normal-Ca group). [Ca2+]i was monitored with fura-2/AM. Increase of preload caused a rise of active tension in hypo-Ca and normal-Ca groups whereas peak fluorescence rose significantly only at low [Ca2+]o. End-diastolic tension, end-diastolic level of fluorescence, time-to-peak tension, but not time-to-peak of Ca2+ transient, progressively increased with preload. Mechanical relaxation decelerated with preload while Ca2+ transient decay time decreased in the initial phase and increased in the late phase, resulting in a prominent “bump” configuration. The “bump” was assessed as a ratio of its area to the fluorescence trace area. It was a new finding that the preload-induced rise of this ratio was twice as large in hypo-Ca. Our results indicate that preload-induced changes in active tension and [Ca2+]i are “dissociated” in rat myocardium, with relatively higher expression at low [Ca2+]o. Ca-dependence of Ca-TnC association/dissociation kinetics is thought to be a main contributor to these preload-induced effects.

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Active Shortening Retards the Decline of the Intracellular Calcium Transient in Mammalian Heart Muscle

Cited by 175 publications

References 24 publications

Effects of bupivacaine, levobupivacaine and ropivacaine on myocardial relaxation

Effects of bupivacaine, levobupivacaine and ropivacaine on myocardial relaxation

Alterations in intracellular calcium and tension of activated ferret papillary muscle in response to step length changes.

Preload-induced changes in isometric tension and [Ca2+]i in rat myocardium

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