Base de dados : MEDLINE
Pesquisa : G02.111.820.800.100.500 [Categoria DeCS]
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[PMID]:29025768
[Au] Autor:Sirish P; Ledford HA; Timofeyev V; Thai PN; Ren L; Kim HJ; Park S; Lee JH; Dai G; Moshref M; Sihn CR; Chen WC; Timofeyeva MV; Jian Z; Shimkunas R; Izu LT; Chiamvimonvat N; Chen-Izu Y; Yamoah EN; Zhang XD
[Ad] Endereço:From the Division of Cardiovascular Medicine, Department of Internal Medicine (P.S., H.A.L., V.T., P.N.T., L.R., S.P., G.D., M.M., C.-R.S., W.C.C., M.V.T., N.C., Y.C.-I., X.-D.Z.), Center for Neuroscience (H.J.K.), Department of Pharmacology (Z.J., R.S., L.T.I., N.C., Y.C.-I.) and Department of Biom
[Ti] Título:Action Potential Shortening and Impairment of Cardiac Function by Ablation of .
[So] Source:Circ Arrhythm Electrophysiol;10(10), 2017 Oct.
[Is] ISSN:1941-3084
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Intracellular pH (pH ) is critical to cardiac excitation and contraction; uncompensated changes in pH impair cardiac function and trigger arrhythmia. Several ion transporters participate in cardiac pH regulation. Our previous studies identified several isoforms of a solute carrier Slc26a6 to be highly expressed in cardiomyocytes. We show that Slc26a6 mediates electrogenic Cl /HCO exchange activities in cardiomyocytes, suggesting the potential role of Slc26a6 in regulation of not only pH , but also cardiac excitability. METHODS AND RESULTS: To test the mechanistic role of Slc26a6 in the heart, we took advantage of knockout ( ) mice using both in vivo and in vitro analyses. Consistent with our prediction of its electrogenic activities, ablation of results in action potential shortening. There are reduced Ca transient and sarcoplasmic reticulum Ca load, together with decreased sarcomere shortening in cardiomyocytes. These abnormalities translate into reduced fractional shortening and cardiac contractility at the in vivo level. Additionally, pH is elevated in cardiomyocytes with slower recovery kinetics from intracellular alkalization, consistent with the Cl /HCO exchange activities of Slc26a6. Moreover, mice show evidence of sinus bradycardia and fragmented QRS complex, supporting the critical role of Slc26a6 in cardiac conduction system. CONCLUSIONS: Our study provides mechanistic insights into Slc26a6, a unique cardiac electrogenic Cl /HCO transporter in ventricular myocytes, linking the critical roles of Slc26a6 in regulation of pH , excitability, and contractility. pH is a critical regulator of other membrane and contractile proteins. Future studies are needed to investigate possible changes in these proteins in mice.
[Mh] Termos MeSH primário: Potenciais de Ação
Antiporters/deficiência
Acoplamento Excitação-Contração
Frequência Cardíaca
Contração Miocárdica
Miócitos Cardíacos/metabolismo
[Mh] Termos MeSH secundário: Animais
Antiporters/genética
Bradicardia/genética
Bradicardia/metabolismo
Bradicardia/fisiopatologia
Células CHO
Cricetulus
Genótipo
Concentração de Íons de Hidrogênio
Cinética
Proteínas de Membrana Transportadoras/genética
Proteínas de Membrana Transportadoras/metabolismo
Camundongos da Linhagem 129
Camundongos Knockout
Fenótipo
Sarcômeros/metabolismo
Retículo Sarcoplasmático/metabolismo
Transfecção
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antiporters); 0 (Membrane Transport Proteins); 0 (SLC26A6 protein, human); 0 (Slc26a6 protein, mouse)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171101
[Lr] Data última revisão:
171101
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE


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[PMID]:28963192
[Au] Autor:Dewenter M; von der Lieth A; Katus HA; Backs J
[Ad] Endereço:From the Department of Molecular Cardiology and Epigenetics (M.D., A.v.d.L., J.B.) and Department of Cardiology (H.A.K.), Heidelberg University, Germany; and DZHK (German Centre for Cardiovascular Research), Partner Site Heidelberg/Mannheim, Germany (M.D., A.v.d.L., H.A.K., J.B.).
[Ti] Título:Calcium Signaling and Transcriptional Regulation in Cardiomyocytes.
[So] Source:Circ Res;121(8):1000-1020, 2017 Sep 29.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Calcium (Ca ) is a universal regulator of various cellular functions. In cardiomyocytes, Ca is the central element of excitation-contraction coupling, but also impacts diverse signaling cascades and influences the regulation of gene expression, referred to as excitation-transcription coupling. Disturbances in cellular Ca -handling and alterations in Ca -dependent gene expression patterns are pivotal characteristics of failing cardiomyocytes, with several excitation-transcription coupling pathways shown to be critically involved in structural and functional remodeling processes. Thus, targeting Ca -dependent transcriptional pathways might offer broad therapeutic potential. In this article, we (1) review cytosolic and nuclear Ca dynamics in cardiomyocytes with respect to their impact on Ca -dependent signaling, (2) give an overview on Ca -dependent transcriptional pathways in cardiomyocytes, and (3) discuss implications of excitation-transcription coupling in the diseased heart.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Cardiopatias/genética
Cardiopatias/metabolismo
Miócitos Cardíacos/metabolismo
Transcrição Genética
[Mh] Termos MeSH secundário: Animais
Sinalização do Cálcio/efeitos dos fármacos
Fármacos Cardiovasculares/uso terapêutico
Núcleo Celular/metabolismo
Citosol/metabolismo
Acoplamento Excitação-Contração
Regulação da Expressão Gênica
Cardiopatias/tratamento farmacológico
Cardiopatias/fisiopatologia
Seres Humanos
Cinética
Contração Miocárdica
Miócitos Cardíacos/efeitos dos fármacos
Transcrição Genética/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Cardiovascular Agents)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171010
[Lr] Data última revisão:
171010
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171001
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.310355


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[PMID]:28778911
[Au] Autor:Yang HY; Firth JM; Francis AJ; Alvarez-Laviada A; MacLeod KT
[Ad] Endereço:National Heart and Lung Institute, Imperial College London, London, United Kingdom; and.
[Ti] Título:Effect of ovariectomy on intracellular Ca regulation in guinea pig cardiomyocytes.
[So] Source:Am J Physiol Heart Circ Physiol;313(5):H1031-H1043, 2017 Nov 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study addressed the hypothesis that long-term deficiency of ovarian hormones after ovariectomy (OVx) alters cellular Ca -handling mechanisms in the heart, resulting in the formation of a proarrhythmic substrate. It also tested whether estrogen supplementation to OVx animals reverses any alterations to cardiac Ca handling and rescues proarrhythmic behavior. OVx or sham operations were performed on female guinea pigs using appropriate anesthetic and analgesic regimes. Pellets containing 17ß-estradiol (1 mg, 60-day release) were placed subcutaneously in selected OVx animals (OVx + E). Cardiac myocytes were enzymatically isolated, and electrophysiological measurements were conducted with a switch-clamp system. In fluo-4-loaded cells, Ca transients were 20% larger, and fractional sarcoplasmic reticulum (SR) Ca release was 7% greater in the OVx group compared with the sham group. Peak L-type Ca current was 16% larger in OVx myocytes with channel inactivation shifting to more positive membrane potentials, creating a larger "window" current. SR Ca stores were 22% greater in the OVx group, and these cells showed a higher frequency of Ca sparks and waves and shorter wave-free intervals. OVx myocytes showed higher frequencies of early afterdepolarizations, and a greater percentage of these cells showed delayed afterdepolarizations after exposure to isoprenaline compared with sham myocytes. The altered Ca regulation occurring in the OVx group was not observed in the OVx + E group. These findings suggest that long-term deprivation of ovarian hormones in guinea pigs lead to changes in myocyte Ca -handling mechanisms that are considered proarrhythmogenic. 17ß-Estradiol replacement prevented these adverse effects. Ovariectomized guinea pig cardiomyocytes have higher frequencies of Ca waves, and isoprenaline-challenged cells display more early afterdepolarizations, delayed afterdepolarizations, and extra beats compared with sham myocytes. These alterations to Ca regulation were not observed in myocytes from ovariectomized guinea pigs supplemented with 17ß-estradiol, suggesting that ovarian hormone deficiency modifies cardiac Ca regulation, potentially creating proarrhythmic substrates.
[Mh] Termos MeSH primário: Sinalização do Cálcio
Cálcio/metabolismo
Miócitos Cardíacos/metabolismo
Ovariectomia
[Mh] Termos MeSH secundário: Potenciais de Ação
Agonistas Adrenérgicos beta/farmacologia
Animais
Arritmias Cardíacas/etiologia
Arritmias Cardíacas/metabolismo
Arritmias Cardíacas/fisiopatologia
Canais de Cálcio Tipo L/genética
Canais de Cálcio Tipo L/metabolismo
Sinalização do Cálcio/efeitos dos fármacos
Implantes de Medicamento
Estradiol/administração & dosagem
Terapia de Reposição de Estrogênios
Acoplamento Excitação-Contração
Feminino
Cobaias
Isoproterenol/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Retículo Sarcoplasmático/metabolismo
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenergic beta-Agonists); 0 (Calcium Channels, L-Type); 0 (Drug Implants); 4TI98Z838E (Estradiol); L628TT009W (Isoproterenol); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171113
[Lr] Data última revisão:
171113
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170806
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00249.2017


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[PMID]:28684623
[Au] Autor:Eisner DA; Caldwell JL; Kistamás K; Trafford AW
[Ad] Endereço:From the Unit of Cardiac Physiology, Division of Cardiovascular Sciences, Manchester Academic Health Sciences Centre, University of Manchester, United Kingdom. eisner@manchester.ac.uk.
[Ti] Título:Calcium and Excitation-Contraction Coupling in the Heart.
[So] Source:Circ Res;121(2):181-195, 2017 Jul 07.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cardiac contractility is regulated by changes in intracellular Ca concentration ([Ca ] ). Normal function requires that [Ca ] be sufficiently high in systole and low in diastole. Much of the Ca needed for contraction comes from the sarcoplasmic reticulum and is released by the process of calcium-induced calcium release. The factors that regulate and fine-tune the initiation and termination of release are reviewed. The precise control of intracellular Ca cycling depends on the relationships between the various channels and pumps that are involved. We consider 2 aspects: (1) structural coupling: the transporters are organized within the dyad, linking the transverse tubule and sarcoplasmic reticulum and ensuring close proximity of Ca entry to sites of release. (2) Functional coupling: where the fluxes across all membranes must be balanced such that, in the steady state, Ca influx equals Ca efflux on every beat. The remainder of the review considers specific aspects of Ca signaling, including the role of Ca buffers, mitochondria, Ca leak, and regulation of diastolic [Ca ] .
[Mh] Termos MeSH primário: Sinalização do Cálcio/fisiologia
Cálcio/fisiologia
Acoplamento Excitação-Contração/fisiologia
Mitocôndrias Cardíacas/fisiologia
Miócitos Cardíacos/fisiologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Líquido Intracelular/fisiologia
Retículo Sarcoplasmático/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
SY7Q814VUP (Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170829
[Lr] Data última revisão:
170829
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170708
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.310230


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[PMID]:28642329
[Au] Autor:Mayourian J; Cashman TJ; Ceholski DK; Johnson BV; Sachs D; Kaji DA; Sahoo S; Hare JM; Hajjar RJ; Sobie EA; Costa KD
[Ad] Endereço:From the Cardiovascular Research Center (J.M., T.J.C., D.K.C., D.S., S.S., R.J.H., K.D.C.), Department of Developmental and Regenerative Biology (D.A.K.), and Department of Pharmacology and Systems Therapeutics (E.A.S.), Icahn School of Medicine at Mount Sinai, New York; Department of Medicine, Univ
[Ti] Título:Experimental and Computational Insight Into Human Mesenchymal Stem Cell Paracrine Signaling and Heterocellular Coupling Effects on Cardiac Contractility and Arrhythmogenicity.
[So] Source:Circ Res;121(4):411-423, 2017 Aug 04.
[Is] ISSN:1524-4571
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Myocardial delivery of human mesenchymal stem cells (hMSCs) is an emerging therapy for treating the failing heart. However, the relative effects of hMSC-mediated heterocellular coupling (HC) and paracrine signaling (PS) on human cardiac contractility and arrhythmogenicity remain unresolved. OBJECTIVE: The objective is to better understand hMSC PS and HC effects on human cardiac contractility and arrhythmogenicity by integrating experimental and computational approaches. METHODS AND RESULTS: Extending our previous hMSC-cardiomyocyte HC computational model, we incorporated experimentally calibrated hMSC PS effects on cardiomyocyte L-type calcium channel/sarcoendoplasmic reticulum calcium-ATPase activity and cardiac tissue fibrosis. Excitation-contraction simulations of hMSC PS-only and combined HC+PS effects on human cardiomyocytes were representative of human engineered cardiac tissue (hECT) contractile function measurements under matched experimental treatments. Model simulations and hECTs both demonstrated that hMSC-mediated effects were most pronounced under PS-only conditions, where developed force increased ≈4-fold compared with non-hMSC-supplemented controls during physiological 1-Hz pacing. Simulations predicted contractility of isolated healthy and ischemic adult human cardiomyocytes would be minimally sensitive to hMSC HC, driven primarily by PS. Dominance of hMSC PS was also revealed in simulations of fibrotic cardiac tissue, where hMSC PS protected from potential proarrhythmic effects of HC at various levels of engraftment. Finally, to study the nature of the hMSC paracrine effects on contractility, proteomic analysis of hECT/hMSC conditioned media predicted activation of PI3K/Akt signaling, a recognized target of both soluble and exosomal fractions of the hMSC secretome. Treating hECTs with exosome-enriched, but not exosome-depleted, fractions of the hMSC secretome recapitulated the effects observed with hMSC conditioned media on hECT-developed force and expression of calcium-handling genes (eg, SERCA2a, L-type calcium channel). CONCLUSIONS: Collectively, this integrated experimental and computational study helps unravel relative hMSC PS and HC effects on human cardiac contractility and arrhythmogenicity, and provides novel insight into the role of exosomes in hMSC paracrine-mediated effects on contractility.
[Mh] Termos MeSH primário: Simulação por Computador
Acoplamento Excitação-Contração/fisiologia
Células Mesenquimais Estromais/fisiologia
Contração Miocárdica/fisiologia
Miócitos Cardíacos/fisiologia
Comunicação Parácrina/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Arritmias Cardíacas/fisiopatologia
Técnicas de Cultura de Células
Diferenciação Celular/fisiologia
Células Cultivadas
Seres Humanos
Camundongos
Ratos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1709
[Cu] Atualização por classe:171116
[Lr] Data última revisão:
171116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170624
[St] Status:MEDLINE
[do] DOI:10.1161/CIRCRESAHA.117.310796


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[PMID]:28609477
[Au] Autor:Whittaker DG; Ni H; El Harchi A; Hancox JC; Zhang H
[Ad] Endereço:Biological Physics Group, School of Physics & Astronomy, The University of Manchester, Manchester, United Kingdom.
[Ti] Título:Atrial arrhythmogenicity of KCNJ2 mutations in short QT syndrome: Insights from virtual human atria.
[So] Source:PLoS Comput Biol;13(6):e1005593, 2017 06.
[Is] ISSN:1553-7358
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Gain-of-function mutations in KCNJ2-encoded Kir2.1 channels underlie variant 3 (SQT3) of the short QT syndrome, which is associated with atrial fibrillation (AF). Using biophysically-detailed human atria computer models, this study investigated the mechanistic link between SQT3 mutations and atrial arrhythmogenesis, and potential ion channel targets for treatment of SQT3. A contemporary model of the human atrial action potential (AP) was modified to recapitulate functional changes in IK1 due to heterozygous and homozygous forms of the D172N and E299V Kir2.1 mutations. Wild-type (WT) and mutant formulations were incorporated into multi-scale homogeneous and heterogeneous tissue models. Effects of mutations on AP duration (APD), conduction velocity (CV), effective refractory period (ERP), tissue excitation threshold and their rate-dependence, as well as the wavelength of re-entry (WL) were quantified. The D172N and E299V Kir2.1 mutations produced distinct effects on IK1 and APD shortening. Both mutations decreased WL for re-entry through a reduction in ERP and CV. Stability of re-entrant excitation waves in 2D and 3D tissue models was mediated by changes to tissue excitability and dispersion of APD in mutation conditions. Combined block of IK1 and IKr was effective in terminating re-entry associated with heterozygous D172N conditions, whereas IKr block alone may be a safer alternative for the E299V mutation. Combined inhibition of IKr and IKur produced a synergistic anti-arrhythmic effect in both forms of SQT3. In conclusion, this study provides mechanistic insights into atrial proarrhythmia with SQT3 Kir2.1 mutations and highlights possible pharmacological strategies for management of SQT3-linked AF.
[Mh] Termos MeSH primário: Arritmias Cardíacas/fisiopatologia
Fibrilação Atrial/fisiopatologia
Acoplamento Excitação-Contração
Sistema de Condução Cardíaco/fisiopatologia
Modelos Cardiovasculares
Canais de Potássio Corretores do Fluxo de Internalização/genética
[Mh] Termos MeSH secundário: Potenciais de Ação
Arritmias Cardíacas/complicações
Fibrilação Atrial/complicações
Simulação por Computador
Predisposição Genética para Doença/genética
Átrios do Coração/fisiopatologia
Seres Humanos
Ativação do Canal Iônico/genética
Modelos Genéticos
Mutação/genética
Contração Miocárdica
Potássio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (KCNJ2 protein, human); 0 (Potassium Channels, Inwardly Rectifying); RWP5GA015D (Potassium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170914
[Lr] Data última revisão:
170914
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pcbi.1005593


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[PMID]:28387534
[Au] Autor:Bayer A; Schmitt S; Günther M; Haeufle DFB
[Ad] Endereço:a Institut für Sport- und Bewegungswissenschaft , Universität Stuttgart , Stuttgart , Germany .
[Ti] Título:The influence of biophysical muscle properties on simulating fast human arm movements.
[So] Source:Comput Methods Biomech Biomed Engin;20(8):803-821, 2017 Jun.
[Is] ISSN:1476-8259
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Computational modeling provides a framework to understand human movement control. For this approach, physiologically motivated and experimentally validated models are required to predict the dynamic interplay of the neuronal controller with the musculoskeletal biophysics. Previous studies show, that an adequate model of arm movements should consider muscle fiber contraction dynamics, parallel and serial elasticities, and activation dynamics. Numerous validated macroscopic model representations of these structures and processes exist. In this study, the influence of these structures and processes on maximum movement velocity of goal-directed arm movements was investigated by varying their mathematical model descriptions. It was found that the movement velocity strongly depends on the pre-activation of the muscles (differences up to 91.6%) and the model representing activation dynamics (differences up to 43.3%). Looking at the influence of the active muscle fibers (contractile element), the simulations reveal that velocities systematically differ depending on the width of the force-length relation (differences up to 17.4%). The series elasticity of the tendon influences the arm velocity up to 7.6%. In conclusion, in fast goal-directed arm movements from an equilibrium position, the modeling of the biophysical muscle properties influences the simulation results. To reliably distinguish between mathematical formulations by experimental validation, the initial muscular activity and the activation dynamics have to be modeled validly, as their influence excels. To this end, further experiments systematically varying the initial muscular activity would be needed.
[Mh] Termos MeSH primário: Braço/fisiologia
Fenômenos Biofísicos
Simulação por Computador
Movimento/fisiologia
Músculo Esquelético/fisiologia
[Mh] Termos MeSH secundário: Fenômenos Biomecânicos
Elasticidade
Cotovelo/fisiologia
Acoplamento Excitação-Contração
Seres Humanos
Modelos Biológicos
Contração Muscular/fisiologia
Músculo Esquelético/inervação
Amplitude de Movimento Articular
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170408
[St] Status:MEDLINE
[do] DOI:10.1080/10255842.2017.1293663


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[PMID]:28357580
[Au] Autor:Temesi J; Mattioni Maturana F; Peyrard A; Piucco T; Murias JM; Millet GY
[Ad] Endereço:Human Performance Laboratory, Faculty of Kinesiology, University of Calgary, 2500 University Drive NW, Calgary, AB, T2N 1N4, Canada.
[Ti] Título:The relationship between oxygen uptake kinetics and neuromuscular fatigue in high-intensity cycling exercise.
[So] Source:Eur J Appl Physiol;117(5):969-978, 2017 May.
[Is] ISSN:1439-6327
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:PURPOSE: In theory, a slow oxygen uptake ([Formula: see text]) kinetics leads to a greater accumulation of anaerobic by-products, which can, in turn, induce more neuromuscular fatigue. However, the existence of this relationship has never been tested. METHODS: After two sessions to measure peak [Formula: see text], peak power output (PO ), and [Formula: see text] kinetics responses in the unfatigued state (τ [Formula: see text] MOD), 10 healthy young adults performed a 6-min cycling bout at 80% PO (INT ). [Formula: see text] kinetics responses were also measured during INT . Neuromuscular fatigue was measured isometrically pre- and post-INT (immediately post- and 15-s post-INT ) with an innovative cycle ergometer. RESULTS: Maximal voluntary contraction (MVC) force, high-frequency doublet amplitude, and the ratio of low- to high-frequency doublet amplitudes decreased by 34 ± 7, 43 ± 11, and 31 ± 13%, respectively (all P < 0.01). A significant Spearman's rank correlation was observed between the change in low-frequency doublet force (ΔDb10) immediately after INT and both τ [Formula: see text] MOD and τ [Formula: see text] INT (ρ = -0.68 and ρ = -0.67, both P < 0.05). When considering the largest responses from the two neuromuscular evaluations post-INT , significant correlations were also found between τ [Formula: see text] MOD and ΔDb10 (ρ = -0.74; P < 0.05) and between τ[Formula: see text] INT and both ΔDb10 and low-frequency fatigue (ρ = -0.70 and ρ = -0.66; both P < 0.05). CONCLUSION: The present results suggest that subjects with slow [Formula: see text] kinetics experience more peripheral fatigue, in particular more excitation-contraction coupling failure, likely due to a greater accumulation of protons and/or inorganic phosphates.
[Mh] Termos MeSH primário: Treinamento Intervalado de Alta Intensidade
Fadiga Muscular
Músculo Esquelético/fisiologia
Consumo de Oxigênio
[Mh] Termos MeSH secundário: Adulto
Acoplamento Excitação-Contração
Feminino
Seres Humanos
Contração Isométrica
Masculino
Músculo Esquelético/inervação
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1706
[Cu] Atualização por classe:171005
[Lr] Data última revisão:
171005
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170331
[St] Status:MEDLINE
[do] DOI:10.1007/s00421-017-3585-1


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[PMID]:28255011
[Au] Autor:Coppini R; Mazzoni L; Ferrantini C; Gentile F; Pioner JM; Laurino A; Santini L; Bargelli V; Rotellini M; Bartolucci G; Crocini C; Sacconi L; Tesi C; Belardinelli L; Tardiff J; Mugelli A; Olivotto I; Cerbai E; Poggesi C
[Ad] Endereço:From the Department NeuroFarBa (R.C., L.M., T.L., L. Santini, V.B., G.B., A.M., E.C.) and Department of Experimental and Clinical Medicine (C.F., F.G., J.M.P., C.T., C.P.), University of Florence, Italy; European Laboratory for Non-linear Spectroscopy (LENS), University of Florence & National In
[Ti] Título:Ranolazine Prevents Phenotype Development in a Mouse Model of Hypertrophic Cardiomyopathy.
[So] Source:Circ Heart Fail;10(3), 2017 03.
[Is] ISSN:1941-3297
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Current therapies are ineffective in preventing the development of cardiac phenotype in young carriers of mutations associated with hypertrophic cardiomyopathy (HCM). Ranolazine, a late Na current blocker, reduced the electromechanical dysfunction of human HCM myocardium in vitro. METHODS AND RESULTS: To test whether long-term treatment prevents cardiomyopathy in vivo, transgenic mice harboring the R92Q troponin-T mutation and wild-type littermates received an oral lifelong treatment with ranolazine and were compared with age-matched vehicle-treated animals. In 12-months-old male R92Q mice, ranolazine at therapeutic plasma concentrations prevented the development of HCM-related cardiac phenotype, including thickening of the interventricular septum, left ventricular volume reduction, left ventricular hypercontractility, diastolic dysfunction, left-atrial enlargement and left ventricular fibrosis, as evaluated in vivo using echocardiography and magnetic resonance. Left ventricular cardiomyocytes from vehicle-treated R92Q mice showed marked excitation-contraction coupling abnormalities, including increased diastolic [Ca ] and Ca waves, whereas cells from treated mutants were undistinguishable from those from wild-type mice. Intact trabeculae from vehicle-treated mutants displayed inotropic insufficiency, increased diastolic tension, and premature contractions; ranolazine treatment counteracted the development of myocardial mechanical abnormalities. In mutant myocytes, ranolazine inhibited the enhanced late Na current and reduced intracellular [Na ] and diastolic [Ca ], ultimately preventing the pathological increase of calmodulin kinase activity in treated mice. CONCLUSIONS: Owing to the sustained reduction of intracellular Ca and calmodulin kinase activity, ranolazine prevented the development of morphological and functional cardiac phenotype in mice carrying a clinically relevant HCM-related mutation. Pharmacological inhibitors of late Na current are promising candidates for an early preventive therapy in young phenotype-negative subjects carrying high-risk HCM-related mutations.
[Mh] Termos MeSH primário: Cardiomiopatia Hipertrófica/prevenção & controle
Miócitos Cardíacos/efeitos dos fármacos
Ranolazina/farmacologia
Bloqueadores dos Canais de Sódio/farmacologia
Sódio/metabolismo
[Mh] Termos MeSH secundário: Animais
Western Blotting
Proteínas Quinases Dependentes de Cálcio-Calmodulina/metabolismo
Cardiomiopatia Hipertrófica/genética
Cardiomiopatia Hipertrófica/metabolismo
Cardiomiopatia Hipertrófica/fisiopatologia
Modelos Animais de Doenças
Ecocardiografia Doppler
Acoplamento Excitação-Contração/efeitos dos fármacos
Predisposição Genética para Doença
Frequência Cardíaca
Hipertrofia Ventricular Esquerda/genética
Hipertrofia Ventricular Esquerda/metabolismo
Hipertrofia Ventricular Esquerda/prevenção & controle
Imagem por Ressonância Magnética
Masculino
Potenciais da Membrana
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Microscopia Confocal
Mutação
Contração Miocárdica/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Miócitos Cardíacos/patologia
Fenótipo
Fatores de Tempo
Troponina T/genética
Disfunção Ventricular Esquerda/genética
Disfunção Ventricular Esquerda/metabolismo
Disfunção Ventricular Esquerda/prevenção & controle
Função Ventricular Esquerda/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Sodium Channel Blockers); 0 (Troponin T); 9NEZ333N27 (Sodium); A6IEZ5M406 (Ranolazine); EC 2.7.11.17 (Calcium-Calmodulin-Dependent Protein Kinases)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170619
[Lr] Data última revisão:
170619
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170304
[St] Status:MEDLINE


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[PMID]:28232646
[Au] Autor:Takei D; Takeshima H
[Ad] Endereço:Graduate School of Pharmaceutical Sciences, Kyoto University, Japan.
[Ti] Título:[Excitation-contraction coupling and junctional membrane structures.]
[So] Source:Clin Calcium;27(3):333-338, 2017.
[Is] ISSN:0917-5857
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:Striated muscle cells form specialized junctional membrane complexes(JMCs)between the cell-surface transverse tubule and sarcoplasmic reticulum(SR)for setting up the excitation-contraction coupling machinery converting depolarization into Ca2+ release signals. Junctophilin subtypes, namely JP1-JP4, are proteins that construct JMCs by binding to the cell membrane and spanning the SR membrane. Recent studies demonstrated that the mutations and altered expression of JP2 take part in cardiac diseases. JPs dominantly affect Ca2+ signaling in striated muscle, and thus may be involved in pathogeneses and progressive pathophysiological conditions in a variety of muscle-related diseases.
[Mh] Termos MeSH primário: Cálcio/metabolismo
Membrana Celular/metabolismo
Acoplamento Excitação-Contração
[Mh] Termos MeSH secundário: Animais
Membrana Celular/química
Seres Humanos
Proteínas de Membrana/metabolismo
Músculo Esquelético/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Membrane Proteins); 0 (junctophilin); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171002
[Lr] Data última revisão:
171002
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170225
[St] Status:MEDLINE
[do] DOI:CliCa1703333338



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