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Relevant bibliographies by topics / Lusitropisme

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Academic literature on the topic 'Lusitropisme'

Author: Grafiati

Published: 4 June 2021

Last updated: 7 February 2022

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Journal articles on the topic "Lusitropisme"

1

Tamiya, Kouichi, Toshiyuki Beppu, and Kazuaki Ishihara. "Double-exponential curve fitting of isometric relaxation: a new measure for myocardial lusitropism." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (1995): 1. http://dx.doi.org/10.1152/ajpheart.1995.269.4.1-a.

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Pages H393–H406: Kouichi Tamiya, Toshiyuki Beppu, and Kazuaki Ishihara. “Double-exponential curve fitting of isometric relaxation: a new measure for myocardial lusitropism.” Page H402: Figure 10 should appear as the following. (See PDF)

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2

Filice, E., T. Angelone, S. Imbrogno, et al. "Beta3-adrenoceptors mediate negative lusitropism via NO-cGMP-PKG pathway." Journal of Molecular and Cellular Cardiology 42, no. 6 (2007): S25. http://dx.doi.org/10.1016/j.yjmcc.2007.03.071.

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3

Mizuno, Ju, Satoshi Mohri, Takeshi Yokoyama, Mikiya Otsuji, Hideko Arita, and Kazuo Hanaoka. "Temperature-dependent inotropic and lusitropic indices based on half-logistic time constants for four segmental phases in isovolumic left ventricular pressure–time curve in excised, cross-circulated canine heart." Canadian Journal of Physiology and Pharmacology 95, no. 2 (2017): 190–98. http://dx.doi.org/10.1139/cjpp-2015-0196.

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Varying temperature affects cardiac systolic and diastolic function and the left ventricular (LV) pressure–time curve (PTC) waveform that includes information about LV inotropism and lusitropism. Our proposed half-logistic (h-L) time constants obtained by fitting using h-L functions for four segmental phases (Phases I–IV) in the isovolumic LV PTC are more useful indices for estimating LV inotropism and lusitropism during contraction and relaxation periods than the mono-exponential (m-E) time constants at normal temperature. In this study, we investigated whether the superiority of the goodness of h-L fits remained even at hypothermia and hyperthermia. Phases I–IV in the isovolumic LV PTCs in eight excised, cross-circulated canine hearts at 33, 36, and 38 °C were analyzed using h-L and m-E functions and the least-squares method. The h-L and m-E time constants for Phases I–IV significantly shortened with increasing temperature. Curve fitting using h-L functions was significantly better than that using m-E functions for Phases I–IV at all temperatures. Therefore, the superiority of the goodness of h-L fit vs. m-E fit remained at all temperatures. As LV inotropic and lusitropic indices, temperature-dependent h-L time constants could be more useful than m-E time constants for Phases I–IV.

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Mizuno, Ju, Satoshi Mohri, Juichiro Shimizu, et al. "Starling-Effect-Independent Lusitropism Index in Canine Left Ventricle: Logistic Time Constant." Anesthesia & Analgesia 102, no. 4 (2006): 1032–39. http://dx.doi.org/10.1213/01.ane.0000202537.19646.10.

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5

Pasqua, Teresa, Angelo Corti, Stefano Gentile, et al. "Full-Length Human Chromogranin-A Cardioactivity: Myocardial, Coronary, and Stimulus-Induced Processing Evidence in Normotensive and Hypertensive Male Rat Hearts." Endocrinology 154, no. 9 (2013): 3353–65. http://dx.doi.org/10.1210/en.2012-2210.

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Plasma chromogranin-A (CgA) concentrations correlate with severe cardiovascular diseases, whereas CgA-derived vasostatin-I and catestatin elicit cardiosuppression via an antiadrenergic/nitric oxide-cGMP mediated mechanism. Whether these phenomena are related is unknown. We here investigated whether and to what extent full-length CgA directly influences heart performance and may be subjected to stimulus-elicited intracardiac processing. Using normotensive and hypertensive rats, we evaluated the following: 1) direct myocardial and coronary effects of full-length CgA; 2) the signal-transduction pathway involved in its action mechanism; and 3) CgA intracardiac processing after β-adrenergic [isoproterenol (Iso)]- and endothelin-1(ET-1)-dependent stimulation. The study was performed by using a Langendorff perfusion apparatus, Western blotting, affinity chromatography, and ELISA. We found that CgA (1–4 nM) dilated coronaries and induced negative inotropism and lusitropism, which disappeared at higher concentrations (10–16 nM). In spontaneously hypertensive rats (SHRs), negative inotropism and lusitropism were more potent than in young normotensive rats. We found that perfusion itself, Iso-, and endothelin-1 stimulation induced intracardiac CgA processing in low-molecular-weight fragments in young, Wistar Kyoto, and SHR rats. In young normotensive and adult hypertensive rats, CgA increased endothelial nitric oxide synthase phosphorylation and cGMP levels. Analysis of the perfusate from both Wistar rats and SHRs of untreated and treated (Iso) hearts revealed CgA absence. In conclusion, in normotensive and hypertensive rats, we evidenced the following: 1) full-length CgA directly affects myocardial and coronary function by AkT/nitric oxide synthase/nitric oxide/cGMP/protein kinase G pathway; and 2) the heart generates intracardiac CgA fragments in response to hemodynamic and excitatory challenges. For the first time at the cardiovascular level, our data provide a conceptual link between systemic and intracardiac actions of full-length CgA and its fragments, expanding the knowledge on the sympathochromaffin/CgA axis under normal and physiopathological conditions.

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6

Tamiya, K., T. Beppu, and K. Ishihara. "Double-exponential curve fitting of isometric relaxation: a new measure for myocardial lusitropism." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 2 (1995): H393—H406. http://dx.doi.org/10.1152/ajpheart.1995.269.2.h393.

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New indexes for evaluation of isometric myocardial relaxation were proposed. In fully isometric and physiologically sequenced twitches, the time course of isometric force decline fitted well with Gompertz's double-exponential curve (r > or = 0.9995). We conformed the original equation to suit myocardial mechanics, i.e., F(t) = gamma 0 - gamma.exp [-alpha.exp (-beta t)] (t = 1, 2, ..., n), where F(t) denotes force as a function of time t. The gamma 0 and gamma relate to upper asymptote and force amplitude, respectively. Phase-plane analysis of F(t) revealed that alpha [3.56 +/- 0.67 (SD)] related to the phasic delay of relaxation onset but did not affect the F(t) vs. dF(t)/dt relation. The beta (0.127 +/- 0.021) and gamma were linearly related to negative dF(t)/dtmax; however, the terminal slope of the phase-plane diagram was governed by beta alone. The tau beta (0.081 +/- 0.017 s), a reciprocal of beta multiplied by sampling time, was practically independent of preload, total load, and muscle shortening. In isometric twitches, tau beta was substantially decreased by global ischemia, isoproterenol, and CaCl2 but increased by reperfusion. The alpha was independent of inotropic interventions but fell significantly during ischemia and was increased by reperfusion.

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7

Takasago, Toshiyuki, Yoichi Goto, Shiho Futaki, et al. "Ejecting volume, filling volume and stroke volume gains: New indexes of inotropism and lusitropism." Heart and Vessels 7, no. 2 (1992): 57–65. http://dx.doi.org/10.1007/bf01744450.

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8

Mizuno, Ju, Junichi Araki, Takeshi Mikane, et al. "Logistic Time Constant of Isometric Relaxation Force Curve of Ferret Ventricular Papillary Muscle. Reliable Index of Lusitropism." Japanese Journal of Physiology 50, no. 5 (2000): 479–87. http://dx.doi.org/10.2170/jjphysiol.50.479.

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9

Ohga, Yoshimi, Susumu Sakata, Chikako Takenaka, et al. "Cardiac dysfunction in terms of left ventricular mechanical work and energetics in hypothyroid rats." American Journal of Physiology-Heart and Circulatory Physiology 283, no. 2 (2002): H631—H641. http://dx.doi.org/10.1152/ajpheart.00046.2002.

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We hypothesized that cardiac dysfunction in hypothyroidism is mainly caused by the impairment of Ca2+ handling in excitation-contraction coupling. To prove this hypothesis, we investigated left ventricular (LV) mechanical work and energetics without interference of preload and afterload in an excised, blood-perfused whole heart preparation from hypothyroid rats. We found that LV inotropism and lusitropism were significantly depressed, and these depressions were causally related to decreased myocardial oxygen consumption for Ca2+ handling and for basal metabolism. The oxygen costs of LV contractility for Ca2+ and for dobutamine in the hypothyroid rats did not differ from those in age-matched normal rats. The expression of sarco(endo)plasmic reticulum Ca2+-ATPase (SERCA2) significantly decreased and that of phospholamban significantly increased. The present results revealed that changes in LV energetics associated with decreased mechanical work in hypothyroid rats are mainly caused by the impairment of Ca2+ uptake via SERCA2. We conclude that the impairment of Ca2+ uptake plays an important role in the pathogenesis of cardiac dysfunction in hypothyroidism.

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10

Angelone, Tommaso, Anna Maria Quintieri, Bhawanjit K. Brar, et al. "The Antihypertensive Chromogranin A Peptide Catestatin Acts as a Novel Endocrine/Paracrine Modulator of Cardiac Inotropism and Lusitropism." Endocrinology 149, no. 10 (2008): 4780–93. http://dx.doi.org/10.1210/en.2008-0318.

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Dissertations / Theses on the topic "Lusitropisme"

1

Hanouz, Jean-Luc. "Effets myocardiques directs des anesthésiques volatils halogénés." Paris 11, 1999. http://www.theses.fr/1999PA11T041.

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Ce travail précise les effets myocardiques directs de deux nouveaux agents anesthésiques volatils halogénés, le sévoflurane et le desflurane, par rapport à l'halothane et l'isoflurane, in vitro, sur le myocarde de rat et le myocarde humain. Nous avons montré que le sévoflurane induit un effet inotrope négatif comparable à celui de l'isoflurane et ne modifie pas les paramètres de lusitropie. Le desflurane induit la libération de catécholamines stockées dans les préparations musculaires isolées. Ces résultats sont importants à considérer puisque le sévoflurane a remplacé l'halothane dans le cadre de l'anesthésie pédiatrique car il permet de réaliser l'induction de l'anesthésie générale au masque avec des effets secondaires cardio-vasculaires et respiratoires moindres que ceux induit par 'halothane. L'utilisation du desflurane pour l'entretien de l'anesthésie générale tend à se généraliser du fait de ses propriétés pharmacocinétiques permettant un réveil plus rapide et de meilleur qualité qu'avec l'isoflurane. Cependant, la libération des catécholamines induite par le desflurane peut, dans certaines circonstances, être délétère pour l'équilibre énergétique du myocarde. La seconde partie de ce travail montre que l'halothane, l'isoflurane et le sévoflurane, aux concentrations utilisées en pratique clinique, potentialisent l'effet inotrope positif d'une stimulation a- et 13-adrénergique. Ces résultats sont à rapprocher des travaux montrant que es anesthésiques volatils halogénés modulent les fonctions des protéines G impliquées dans la transduction du signal a- et 13-adrénergique. Ces résultats sont importants car le médecin anesthésiste-réanimateur doit prendre en charge des patients à l'équilibre hémodynamique fragile nécessitant l'administration de catécholamines ou atteint de pathologies caractérisées par des taux plasmatiques élevés de catécholamines endogènes et/ou une activation importante du système sympathique. Enfin, les modifications constitutionnelles ou acquises du système des protéines G sont impliquées dans de nombreuses circonstances physiopathologiques.

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2

Clergue, Michel. "Effets de la chlorpromazine sur l'inotropie, la lusitropie et l'économie myocardiques : étude in vitro sur muscle papillaire ventriculaire gauche de rat." Paris 11, 1993. http://www.theses.fr/1993PA112093.

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La calmoduline (CaM) est une protéine calcium-dépendante ubiquitaire responsable de la modulation d'un grand nombre d'activités cellulaires enzymatiques, en particulier au niveau myocardique. L'activité de la CaM est inhibée par les phénothiazines, notamment la Chlorpromazine (CPZ). Cette étude permet de mieux caractériser l'impact mécanique et énergétique d'un agent neuroleptique sur le muscle papillaire isolé, dans des conditions d'isotonie et d'isométrie. Les altérations majeures induites par des doses croissantes de CPZ sur l'inotropie, la lusitropie, le couplage contraction-relaxation et l'énergétique évoquent principalement une action inhibitrice sur les capacités de recaptage du calcium par le réticulum sarcoplasmique, conséquence de l'effet anti-CaM de la CPZ. D'autres mécanismes à l'échelon cellulaire, comme la réduction de la sensibilité au calcium des myofilaments, l'inhibition de la troponine C, et la modification des cinétiques des ponts actine-myosine semblent être également impliqués, comme le montre l'effet délétère thermo-énergétique constaté à forte dose. Ces résultats sont en faveur d'une dysrégulation de l'homéostasie calcique intramyoplasmique dans le syndrome malin des neuroleptiques (SMN). Du fait des similarités cliniques et thérapeutiques entre SMN et hyperthermie maligne des anesthésiques, des mécanismes physiopathologiques communs peuvent être évoqués.

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3

Langeron, Olivier. "Physiologie et pharmacologie normale et pathologique du muscle diaphragmatique isolé." Paris 6, 2002. http://www.theses.fr/2002PA066208.

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4

Orliaguet, Gilles. "Effets diaphragmatiques des médicaments utilisés en anesthésie au cours du développement postnatal." Paris 6, 2002. http://www.theses.fr/2002PA066278.

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5

Desjardins, Jean-François. "Effets protecteurs d'un donneur de NO sur la fonction diastolique du coeur défaillant de hamster UM-X7.1." Thèse, 2003. http://hdl.handle.net/1866/15042.

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