Real-time kinetics of sarcomere relaxation by laser diffraction.

Lecarpentier, Yves; Martin, Jean−Louis; Claes, Victor; Chambaret, Jean-Paul; Migus, A.; Antonetti, A.; Hatt, P. Y.

doi:10.1161/01.res.56.3.331

Cited by 51 publications

(25 citation statements)

References 32 publications

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“…Most laser diffraction sarcomere control systems only record the position of one of the first order diffraction peaks (e.g., [64,65]). These studies assume that both left and right first order peaks move equally during changes in SL and that the zero order peak position remains fixed in position.…”

Section: Methodsmentioning

confidence: 99%

X-ray Diffraction Evidence for Low Force Actin-Attached and Rigor-Like Cross-Bridges in the Contractile Cycle

Eakins

Pinali²,

Gleeson

et al. 2016

Biology

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Defining the structural changes involved in the myosin cross-bridge cycle on actin in active muscle by X-ray diffraction will involve recording of the whole two dimensional (2D) X-ray diffraction pattern from active muscle in a time-resolved manner. Bony fish muscle is the most highly ordered vertebrate striated muscle to study. With partial sarcomere length (SL) control we show that changes in the fish muscle equatorial A-band (10) and (11) reflections, along with (10)/(11) intensity ratio and the tension, are much more rapid than without such control. Times to 50% change with SL control were 19.5 (±2.0) ms, 17.0 (±1.1) ms, 13.9 (±0.4) ms and 22.5 (±0.8) ms, respectively, compared to 25.0 (±3.4) ms, 20.5 (±2.6) ms, 15.4 (±0.6) ms and 33.8 (±0.6) ms without control. The (11) intensity and the (10)/(11) intensity ratio both still change ahead of tension, supporting the likelihood of the presence of a head population close to or on actin, but producing little or no force, in the early stages of the contractile cycle. Higher order equatorials (e.g., (30), (31), and (32)), more sensitive to crossbridge conformation and distribution, also change very rapidly and overshoot their tension plateau values by a factor of around two, well before the tension plateau has been reached, once again indicating an early low-force cross-bridge state in the contractile cycle. Modelling of these intensity changes suggests the presence of probably two different actin-attached myosin head structural states (mainly low-force attached and rigor-like). No more than two main attached structural states are necessary and sufficient to explain the observations. We find that 48% of the heads are off actin giving a resting diffraction pattern, 20% of heads are in the weak binding conformation and 32% of the heads are in the strong (rigor-like) state. The strong states account for 96% of the tension at the tetanus plateau.

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Section: Methodsmentioning

confidence: 99%

X-ray Diffraction Evidence for Low Force Actin-Attached and Rigor-Like Cross-Bridges in the Contractile Cycle

Eakins

Pinali²,

Gleeson

et al. 2016

Biology

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“…22 When the muscle contracts isometrically, sarcomeres shorten very little. 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.…”

Section: Mechanical Parametersmentioning

confidence: 99%

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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“…This is of interest considering the mechanical differences observed during a similar chronic pressure overload induced in guinea pig and in rat, particularly when the relaxation phase is analyzed. 42 …”

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confidence: 99%

Major alterations in relaxation during cardiac hypertrophy induced by aortic stenosis in guinea pig.

Lecarpentier¹,

Waldenström²,

Clergue³

et al. 1987

Circulation Research

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Left ventricular hypertrophy (LVH) was produced in guinea pigs after aortic stenosis (AS). The percentage of LVH in AS was determined by normalizing left ventricular (LY) weight by the mean LV weight of sham-operated controls (n = 12). After 3 weeks of cardiac overload, a mild LVH (30 ± 3%) was induced in 17 animals and a relatively severe LVH (56 ±3%) was induced in 7 animals. LV papillary muscles were rapidly excised for mechanical studies. No significant differences were observed between control and mild hypertrophy groups. In contrast, a marked decrease in myocardial performance was seen in the more severe cardiac hypertrophy group and was expressed as a percentage of sham-operated levels (Vmax, 22%; active isometric force/mm 2 ,23%; + dF/dt max/mm 2 ,26%). Relaxation in this group was still more impaired than contraction (peak lengthening velocity, 14%; -dF/dt max/mm 2 , 19%). Moreover, the load sensitivity of relaxation was present in both shamoperated controls and mild hypertrophy but almost disappeared in more severe hypertrophy. Isometric relaxation was delayed in the latter group, as shown by the 15% increase of the half-time of the decline of isometric relaxation (t w ). On the other hand, acute hypoxia (95% N 2 -5% CO 2 for 20 minutes) also induced a fall in contractility and the disappearance of the load sensitivity of relaxation but with a 67% decrease of ti.. Thus, the mechanical analysis of relaxation allows the effects of chronic overload in relatively severe cardiac hypertrophy to be separated from those of acute hypoxia. Moreover, in severe cardiac hypertrophy, the impairment of the load sensitivity of relaxation with increased ti/, strongly suggests alterations of the sarcoplasmic reticulum. especially since the moderate decrease in the myofibrillar ATPase activity, which has been observed previously in guinea pig pressure overload, cannot account completely for the marked fall in myocardial performance. (Circulation Research 1987;61:I07-116) C hronic cardiac overload appears to modify the myocyte homeostasis in a complex manner, as shown by numerous biochemical, metabolic, or mechanical alterations described in the literature, These changes observed during cardiac hypertrophy are, in part, species specific. Thus, the rat myocardium adapts to chronic overload by changing the fast V, isomyosin to the slow V,, 1 and this isomyosin shift is related linearly to alterations in contractility 21 Also, it has been shown that relaxation in the hypertrophied rat myocardium remains sensitive to the loading conditions, a mechanical property that generally seems to be present when the sarcoplasmic reticulum is normally functional and that, in the rat, is never impaired, whatever the degree or type of cardiac overload.

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Real-time kinetics of sarcomere relaxation by laser diffraction.

Cited by 51 publications

References 32 publications

X-ray Diffraction Evidence for Low Force Actin-Attached and Rigor-Like Cross-Bridges in the Contractile Cycle

X-ray Diffraction Evidence for Low Force Actin-Attached and Rigor-Like Cross-Bridges in the Contractile Cycle

Effects of bupivacaine, levobupivacaine and ropivacaine on myocardial relaxation

Major alterations in relaxation during cardiac hypertrophy induced by aortic stenosis in guinea pig.

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