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[PMID]:29191327
[Au] Autor:Yu L; Zhou L; Cao G; Po SS; Huang B; Zhou X; Wang M; Yuan S; Wang Z; Wang S; Jiang H
[Ad] Endereço:Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan, China; Cardiovascular Research Institute, Wuhan University, Wuhan, China; Hubei Key Laboratory of Cardiology, Wuhan, China.
[Ti] Título:Optogenetic Modulation of Cardiac Sympathetic Nerve Activity to Prevent Ventricular Arrhythmias.
[So] Source:J Am Coll Cardiol;70(22):2778-2790, 2017 Dec 05.
[Is] ISSN:1558-3597
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Studies have shown that left stellate ganglion (LSG) suppression protects against ventricular arrhythmias (VAs). Optogenetics is a novel technique to reversibly regulate the activity of the targeted neurons. OBJECTIVES: This study aimed to investigate whether an optogenetically silenced LSG could protect against VAs induced by myocardial ischemia. METHODS: Adeno-associated virus (AAV) was used as the vector to deliver ArchT, an inhibitory light-sensitive opsin, to the LSG neurons. Twenty male beagles were randomized into the optogenetics group (n = 10, AAV2/9-CAG-ArchT-GFP microinjected into LSG) and control group (n = 10, AAV2/9-CAG-GFP microinjected into LSG). After 4 weeks, the LSG function and neural activity, heart rate variability, ventricular action potential duration, and effective refractory period were measured in the absence or presence of a light-emitting diode illumination (565 nm). Myocardial ischemia was induced by left anterior coronary artery ligation and 1 h of electrocardiography was recorded for VAs analysis. RESULTS: ArchT was successfully expressed in all dogs. Transient light-emitting diode illumination significantly suppressed the LSG function, LSG neural activity, and sympathetic nerve indices of heart rate variability as well as prolonged left ventricular effective refractory period and APD90 only in the optogenetics group. Thirty-minute illumination further enhanced these changes in the optogenetics group. Importantly, all of these changes returned to baseline within 2 h after illumination was turned off. Moreover, the ischemia-induced VAs were significantly suppressed by illumination only in the optogenetics group. CONCLUSIONS: Optogenetic modulation could reversibly inhibit the neural activity of LSG, thereby increasing electrophysiological stability and protecting against myocardial ischemia-induced VAs.
[Mh] Termos MeSH primário: Sistema de Condução Cardíaco/fisiopatologia
Isquemia Miocárdica
Optogenética/métodos
Taquicardia Ventricular
[Mh] Termos MeSH secundário: Potenciais de Ação/fisiologia
Animais
Modelos Animais de Doenças
Cães
Eletrocardiografia/métodos
Frequência Cardíaca
Masculino
Isquemia Miocárdica/complicações
Isquemia Miocárdica/fisiopatologia
Período Refratário Eletrofisiológico/fisiologia
Gânglio Estrelado/fisiologia
Taquicardia Ventricular/etiologia
Taquicardia Ventricular/fisiopatologia
Taquicardia Ventricular/prevenção & controle
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171205
[Lr] Data última revisão:
171205
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE


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[PMID]:29038102
[Au] Autor:Leong KMW; Ng FS; Yao C; Roney C; Taraborrelli P; Linton NWF; Whinnett ZI; Lefroy DC; Davies DW; Boon Lim P; Harding SE; Peters NS; Kanagaratnam P; Varnava AM
[Ad] Endereço:From the National Heart and Lung Institute, Imperial College London, United Kingdom (K.M.W.L., F.S.N., C.R., N.W.F.L., Z.I.W., P.B.L., S.E.H., N.S.P., P.K.); Imperial College Healthcare NHS Trust, London, United Kingdom (K.M.W.L., F.S.N., P.T., N.W.F.L., Z.I.W., D.C.L., D.W.D., P.B.L., N.S.P., P.K.,
[Ti] Título:ST-Elevation Magnitude Correlates With Right Ventricular Outflow Tract Conduction Delay in Type I Brugada ECG.
[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: The substrate location and underlying electrophysiological mechanisms that contribute to the characteristic ECG pattern of Brugada syndrome (BrS) are still debated. Using noninvasive electrocardiographical imaging, we studied whole heart conduction and repolarization patterns during ajmaline challenge in BrS individuals. METHODS AND RESULTS: A total of 13 participants (mean age, 44±12 years; 8 men), 11 concealed patients with type I BrS and 2 healthy controls, underwent an ajmaline infusion with electrocardiographical imaging and ECG recordings. Electrocardiographical imaging activation recovery intervals and activation timings across the right ventricle (RV) body, outflow tract (RVOT), and left ventricle were calculated and analyzed at baseline and when type I BrS pattern manifested after ajmaline infusion. Peak J-ST point elevation was calculated from the surface ECG and compared with the electrocardiographical imaging-derived parameters at the same time point. After ajmaline infusion, the RVOT had the greatest increase in conduction delay (5.4±2.8 versus 2.0±2.8 versus 1.1±1.6 ms; =0.007) and activation recovery intervals prolongation (69±32 versus 39±29 versus 21±12 ms; =0.0005) compared with RV or left ventricle. In controls, there was minimal change in J-ST point elevation, conduction delay, or activation recovery intervals at all sites with ajmaline. In patients with BrS, conduction delay in RVOT, but not RV or left ventricle, correlated to the degree of J-ST point elevation (Pearson , 0.81; <0.001). No correlation was found between J-ST point elevation and activation recovery intervals prolongation in the RVOT, RV, or left ventricle. CONCLUSIONS: Magnitude of ST (J point) elevation in the type I BrS pattern is attributed to degree of conduction delay in the RVOT and not prolongation in repolarization time.
[Mh] Termos MeSH primário: Potenciais de Ação
Mapeamento Potencial de Superfície Corporal
Síndrome de Brugada/diagnóstico
Eletrocardiografia
Sistema de Condução Cardíaco/fisiopatologia
Frequência Cardíaca
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Adulto
Ajmalina/administração & dosagem
Antiarrítmicos/administração & dosagem
Síndrome de Brugada/fisiopatologia
Estudos de Casos e Controles
Feminino
Sistema de Condução Cardíaco/efeitos dos fármacos
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
Masculino
Meia-Idade
Valor Preditivo dos Testes
Período Refratário Eletrofisiológico
Processamento de Sinais Assistido por Computador
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 1PON08459R (Ajmaline)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171023
[Lr] Data última revisão:
171023
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171018
[St] Status:MEDLINE


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[PMID]:29018164
[Au] Autor:Diness JG; Skibsbye L; Simó-Vicens R; Santos JL; Lundegaard P; Citerni C; Sauter DRP; Bomholtz SH; Svendsen JH; Olesen SP; Sørensen US; Jespersen T; Grunnet M; Bentzen BH
[Ad] Endereço:From the Acesion Pharma, Copenhagen, Denmark (J.G.D., R.S.-V., C.C., D.R.P.S., S.H.B., U.S.S., M.G., B.H.B.); Department of Biomedical Sciences, Faculty of Health and Medical Sciences, University of Copenhagen, Denmark (L.S., J.L.S., P.L., D.R.P.S., S.-P.O., T.J., M.G., B.H.B.); and the Heart Centre
[Ti] Título:Termination of Vernakalant-Resistant Atrial Fibrillation by Inhibition of Small-Conductance Ca -Activated K Channels in Pigs.
[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: Evidence has emerged that small-conductance Ca -activated K (SK) channels constitute a new target for treatment of atrial fibrillation (AF). SK channels are predominantly expressed in the atria as compared with the ventricles. Various marketed antiarrhythmic drugs are limited by ventricular adverse effects and efficacy loss as AF progresses. METHODS AND RESULTS: A total of 43 pigs were used for the studies. AF reversion in conscious long-term tachypaced pigs: Pigs were subjected to atrial tachypacing (7 Hz) until they developed sustained AF that could not be reverted by vernakalant 4 mg/kg (18.8±3.3 days of atrial tachypacing). When the SK channel inhibitor AP14145 was tested in these animals, vernakalant-resistant AF was reverted to sinus rhythm, and reinduction of AF by burst pacing (50 Hz) was prevented in 8 of 8 pigs. Effects on refractory period and AF duration in open chest pigs: The effects of AP14145 and vernakalant on the effective refractory periods and acute burst pacing-induced AF were examined in anaesthetized open chest pigs. Both vernakalant and AP14145 significantly prolonged atrial refractoriness and reduced AF duration without affecting the ventricular refractoriness or blood pressure in pigs subjected to 7 days atrial tachypacing, as well as in sham-operated control pigs. CONCLUSIONS: SK currents play a role in porcine atrial repolarization, and pharmacological inhibition of these with AP14145 demonstrates antiarrhythmic effects in a vernakalant-resistant porcine model of AF. These results suggest SK channel blockers as potentially interesting anti-AF drugs.
[Mh] Termos MeSH primário: Anisóis/farmacologia
Fibrilação Atrial/tratamento farmacológico
Fibrilação Atrial/fisiopatologia
Pirrolidinas/farmacologia
Canais de Potássio Ativados por Cálcio de Condutância Baixa/antagonistas & inibidores
[Mh] Termos MeSH secundário: Acetamidas
Animais
Estimulação Cardíaca Artificial
Modelos Animais de Doenças
Progressão da Doença
Técnicas de Patch-Clamp
Período Refratário Eletrofisiológico
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (AP14145); 0 (Acetamides); 0 (Anisoles); 0 (Pyrrolidines); 0 (Small-Conductance Calcium-Activated Potassium Channels); 9G468C8B13 (vernakalant)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171012
[St] Status:MEDLINE


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[PMID]:28381818
[Au] Autor:Saengklub N; Limprasutr V; Sawangkoon S; Hamlin RL; Kijtawornrat A
[Ad] Endereço:Animal Physiology Program, Faculty of Veterinary Science, Chulalongkorn University, 39 Henri Dunant Road, Pathumwan, Bangkok 10330, Thailand.
[Ti] Título:Dronedarone attenuates the duration of atrial fibrillation in a dog model of sustained atrial fibrillation.
[So] Source:Exp Anim;66(3):251-258, 2017 Aug 05.
[Is] ISSN:1881-7122
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Atrial fibrillation (AF) is a supraventricular arrhythmia that leads to a decrease in cardiac output and impairs cardiac function and quality of life. Dronedarone has an atrial-selective property and has been used for management of AF in humans, but limited information is available in dogs. This study was designed to evaluate efficacy of dronedarone in attenuating the duration of AF in dog model of sustained AF. Six beagle dogs were anesthetized with isoflurane and instrumented to measure atrial action potential duration (aAPD) and atrial effective refractory period (AERP). Then AF was induced by rapid right atrial pacing (20 V, 40 Hz) simultaneously with infusion of phenylephrine (2 µg/kg/min, intravenously) for 20 min. The duration of sustained AF was recorded, and the animals were allowed to recover. Dronedarone was given at a dose of 20 mg/kg, BID, orally for 7 days. On the last day, the dogs were anesthetized again to record aAPD and AERP, and AF was induced with the same procedure as described above. The results showed that after dronedarone administration the aAPD was lengthened significantly from 76.4 ± 4.2 ms to 91.2 ± 3.9 ms (P<0.05) and AERP was prolonged significantly from 97.5 ± 2.8 ms to 120 ± 4.8 ms (P<0.05). The duration of sustained AF was also significantly attenuated after receipt of dronedarone (P<0.05). It can be suggested that oral dronedarone attenuates the duration of sustained AF in a dog model of AF by extending the AERP more than the aAPD, causing post-repolarization refractoriness. Hence, dronedarone may be useful for management of AF in dogs.
[Mh] Termos MeSH primário: Amiodarona/análogos & derivados
Fibrilação Atrial/tratamento farmacológico
Modelos Animais de Doenças
Cães
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Administração Oral
Amiodarona/administração & dosagem
Amiodarona/farmacologia
Animais
Fibrilação Atrial/fisiopatologia
Átrios do Coração/fisiopatologia
Seres Humanos
Período Refratário Eletrofisiológico/efeitos dos fármacos
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
JQZ1L091Y2 (dronedarone); N3RQ532IUT (Amiodarone)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170928
[Lr] Data última revisão:
170928
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170407
[St] Status:MEDLINE
[do] DOI:10.1538/expanim.17-0002


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[PMID]:28231318
[Au] Autor:Osadchii OE
[Ad] Endereço:Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
[Ti] Título:Effects of Na+ channel blockers on the restitution of refractory period, conduction time, and excitation wavelength in perfused guinea-pig heart.
[So] Source:PLoS One;12(2):e0172683, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Na+ channel blockers flecainide and quinidine can increase propensity to ventricular tachyarrhythmia, whereas lidocaine and mexiletine are recognized as safe antiarrhythmics. Clinically, ventricular fibrillation is often precipitated by transient tachycardia that reduces action potential duration, suggesting that a critical shortening of the excitation wavelength (EW) may contribute to the arrhythmic substrate. This study examined whether different INa blockers can produce contrasting effects on the rate adaptation of the EW, which would explain the difference in their safety profile. In perfused guinea-pig hearts, effective refractory periods (ERP), conduction times, and EW values were determined over a wide range of cardiac pacing intervals. All INa blockers tested were found to flatten the slope of ERP restitution, indicating antiarrhythmic tendency. However, with flecainide and quinidine, the beneficial changes in ERP were reversed owing to the use-dependent conduction slowing, thereby leading to significantly steepened restitution of the EW. In contrast, lidocaine and mexiletine had no effect on ventricular conduction, and therefore reduced the slope of the EW restitution, as expected from their effect on ERP. These findings suggest that the slope of the EW restitution is an important electrophysiological determinant which can discriminate INa blockers with proarrhythmic and antiarrhythmic profile.
[Mh] Termos MeSH primário: Flecainida/farmacologia
Sistema de Condução Cardíaco/efeitos dos fármacos
Coração/efeitos dos fármacos
Quinidina/farmacologia
Período Refratário Eletrofisiológico/efeitos dos fármacos
Bloqueadores do Canal de Sódio Disparado por Voltagem/farmacologia
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Eletrocardiografia
Feminino
Cobaias
Frequência Cardíaca/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Voltage-Gated Sodium Channel Blockers); ITX08688JL (Quinidine); K94FTS1806 (Flecainide)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170224
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172683


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[PMID]:28039911
[Au] Autor:Frommeyer G; Sterneberg M; Dechering DG; Kaese S; Bögeholz N; Pott C; Fehr M; Bogossian H; Milberg P; Eckardt L
[Ad] Endereço:Division of Clinical and Experimental Electrophysiology, Department of Cardiology and Angiology, University Hospital of Münster, Münster, Germany.
[Ti] Título:Effective suppression of atrial fibrillation by the antihistaminic agent antazoline: First experimental insights into a novel antiarrhythmic agent.
[So] Source:Cardiovasc Ther;35(2), 2017 Apr.
[Is] ISSN:1755-5922
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: The antihistaminic antazoline (ANT) was reported to be highly effective and safe for rapid conversion of atrial fibrillation (AF). We therefore analyzed underlying mechanisms in an experimental whole-heart model. METHODS AND RESULTS: Isolated and retrogradely perfused rabbit hearts underwent a standardized protocol employing atrial burst pacing-induced AF in five of 20 hearts under baseline conditions (seven episodes). Thereafter, a combination of acetylcholine and isoproterenol was employed to enhance AF occurrence. Two monophasic action potential recordings on the left- and two on the right atrial epicardium showed a decrease in atrial action potential duration (aAPD, -25 msec, P<.05) and atrial effective refractory period (aERP; -52 msec, P<.01) after infusion of acetylcholine (1 µmol/L) and isoproterenol (1 µmol/L). This led to induction of AF in 14 of 20 hearts (145 episodes). Simultaneous infusion of ANT (20 µmol/L) led to a complete suppression of AF in all inducible hearts. Treatment with ANT also led to a significant increase in aAPD (+41 msec, P<.01) and aERP (+74 msec, P<.05), leading to a marked increase in atrial postrepolarization refractoriness (aPRR, +33 msec, P<.01). Results were compared to 13 rabbits treated with flecainide. Flecainide induced a significant increase in aPRR and resulted in induction of AF in seven of 13 hearts (51 episodes) while 11 of 13 hearts were inducible with acetylcholine and isoproterenol (93 episodes). CONCLUSION: Administration of ANT was highly effective in suppressing AF. The antiarrhythmic effect could be explained by a significant increase in postrepolarization refractoriness as a result of a more marked increase in aERP as compared with aAPD.
[Mh] Termos MeSH primário: Antazolina/farmacologia
Antiarrítmicos/farmacologia
Fibrilação Atrial/prevenção & controle
Frequência Cardíaca/efeitos dos fármacos
Antagonistas dos Receptores Histamínicos H1/farmacologia
[Mh] Termos MeSH secundário: Acetilcolina
Potenciais de Ação
Animais
Fibrilação Atrial/induzido quimicamente
Fibrilação Atrial/fisiopatologia
Estimulação Cardíaca Artificial
Relação Dose-Resposta a Droga
Descoberta de Drogas
Eletrocardiografia
Técnicas Eletrofisiológicas Cardíacas
Flecainida/farmacologia
Preparação de Coração Isolado
Isoproterenol
Coelhos
Período Refratário Eletrofisiológico
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Histamine H1 Antagonists); DHA8014SS1 (Antazoline); K94FTS1806 (Flecainide); L628TT009W (Isoproterenol); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170327
[Lr] Data última revisão:
170327
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170101
[St] Status:MEDLINE
[do] DOI:10.1111/1755-5922.12244


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[PMID]:28011584
[Au] Autor:Rossi S; Buccarello A; Ershler PR; Lux RL; Callegari S; Corradi D; Carnevali L; Sgoifo A; Miragoli M; Musso E; Macchi E
[Ad] Endereço:Department of Life Sciences, Università degli Studi, Parma, Italy.
[Ti] Título:Effect of anisotropy on ventricular vulnerability to unidirectional block and reentry by single premature stimulation during normal sinus rhythm in rat heart.
[So] Source:Am J Physiol Heart Circ Physiol;312(3):H584-H607, 2017 Mar 01.
[Is] ISSN:1522-1539
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Single high-intensity premature stimuli when applied to the ventricles during ventricular drive of an ectopic site, as in Winfree's "pinwheel experiment," usually induce reentry arrhythmias in the normal heart, while single low-intensity stimuli barely do. Yet ventricular arrhythmia vulnerability during normal sinus rhythm remains largely unexplored. With a view to define the role of anisotropy on ventricular vulnerability to unidirectional conduction block and reentry, we revisited the pinwheel experiment with reduced constraints in the in situ rat heart. New features included single premature stimulation during normal sinus rhythm, stimulation and unipolar potential mapping from the same high-resolution epicardial electrode array, and progressive increase in stimulation strength and prematurity from diastolic threshold until arrhythmia induction. Measurements were performed with 1-ms cathodal stimuli at multiple test sites ( = 26) in seven rats. Stimulus-induced virtual electrode polarization during sinus beat recovery phase influenced premature ventricular responses. Specifically, gradual increase in stimulus strength and prematurity progressively induced make, break, and graded-response stimulation mechanisms. Hence unidirectional conduction block occurred as follows: ) along fiber direction, on right and left ventricular free walls ( = 23), initiating figure-eight reentry ( = 17) and tachycardia ( = 12), and ) across fiber direction, on lower interventricular septum ( = 3), initiating spiral wave reentry ( = 2) and tachycardia ( = 1). Critical time window (55.1 ± 4.7 ms, 68.2 ± 6.0 ms) and stimulus strength lower limit (4.9 ± 0.6 mA) defined vulnerability to reentry. A novel finding of this study was that ventricular tachycardia evolves and is maintained by episodes of scroll-like wave and focal activation couplets. We also found that single low-intensity premature stimuli can induce repetitive ventricular response ( = 13) characterized by focal activations. We performed ventricular cathodal point stimulation during sinus rhythm by progressively increasing stimulus strength and prematurity. Virtual electrode polarization and recovery gradient progressively induced make, break, and graded-response stimulation mechanisms. Unidirectional conduction block occurred along or across fiber direction, initiating figure-eight or spiral wave reentry, respectively, and tachycardia sustained by scroll wave and focal activations.
[Mh] Termos MeSH primário: Ventrículos do Coração/efeitos dos fármacos
Ventrículos do Coração/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Anisotropia
Arritmia Sinusal
Estimulação Elétrica
Eletrodos
Mapeamento Epicárdico
Bloqueio Cardíaco/fisiopatologia
Sistema de Condução Cardíaco/efeitos dos fármacos
Septos Cardíacos/fisiopatologia
Ratos
Período Refratário Eletrofisiológico
Taquicardia por Reentrada no Nó Sinoatrial/fisiopatologia
Taquicardia Ventricular/fisiopatologia
Função Ventricular Esquerda
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161225
[St] Status:MEDLINE
[do] DOI:10.1152/ajpheart.00366.2016


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[PMID]:27390180
[Au] Autor:Monk S; Leib H
[Ti] Título:A Model for Single Neuron Activity With Refractory Effects and Spike Rate Estimation Techniques.
[So] Source:IEEE Trans Neural Syst Rehabil Eng;25(4):306-322, 2017 Apr.
[Is] ISSN:1558-0210
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The use of random point processes as models for neural spike trains allows the derivation of powerful statistical estimation techniques for time varying firing rates. Frequently, however, such estimators are based on the assumption that spike sequences follow a Poisson point process. Because of the bio-physical properties of neuronal action potentials, spike trains are affected by the refractory phenomenon that induces history dependency, and hence contradicts the Poisson assumption. In this work we present a neural spiking model, and a Maximum Likelihood (ML) estimation framework for time varying firing rates, that account for history dependencies in spike trains. Our framework is based on an exponential of polynomial model for the excitation function (stimulus), that generates a self exciting point process representing spike trains with absolute as well as relative refractory effects. Using this framework we employ techniques based on non-convex optimization and model order selection to derive ML estimators for neuronal firing rates. Results on simulated data with a refractory period show an improvement in accuracy when our estimation technique, that accounts for the complete refractory phenomenon, is used. Employing this estimation method for measured neuronal data shows an improvement in goodness of fit over estimators that do not account for the refractory effect, and also over other commonly used techniques.
[Mh] Termos MeSH primário: Potenciais de Ação/fisiologia
Modelos Neurológicos
Modelos Estatísticos
Neurônios/fisiologia
Período Refratário Eletrofisiológico/fisiologia
[Mh] Termos MeSH secundário: Animais
Simulação por Computador
Seres Humanos
Reprodutibilidade dos Testes
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170713
[Lr] Data última revisão:
170713
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160709
[St] Status:MEDLINE
[do] DOI:10.1109/TNSRE.2016.2586659


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[PMID]:27140189
[Au] Autor:Moreira-Lobo DC; Cruz JS; Silva FR; Ribeiro FM; Kushmerick C; Oliveira FA
[Ad] Endereço:Department of Biochemistry and Immunology, Institute of Biological Sciences, Universidade Federal de Minas Gerais, Avenida Antônio Carlos, 6627, Bloco K4, Sala #167, Belo Horizonte, MG, CEP 31270-901, Brazil.
[Ti] Título:Thiamine Deficiency Increases Ca Current and Ca 1.2 L-type Ca Channel Levels in Cerebellum Granular Neurons.
[So] Source:Cell Mol Neurobiol;37(3):453-460, 2017 Apr.
[Is] ISSN:1573-6830
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Thiamine (vitamin B1) is co-factor for three pivotal enzymes for glycolytic metabolism: pyruvate dehydrogenase, α-ketoglutarate dehydrogenase, and transketolase. Thiamine deficiency leads to neurodegeneration of several brain regions, especially the cerebellum. In addition, several neurodegenerative diseases are associated with impairments of glycolytic metabolism, including Alzheimer's disease. Therefore, understanding the link between dysfunction of the glycolytic pathway and neuronal death will be an important step to comprehend the mechanism and progression of neuronal degeneration as well as the development of new treatment for neurodegenerative states. Here, using an in vitro model to study the effects of thiamine deficiency on cerebellum granule neurons, we show an increase in Ca current density and Ca 1.2 expression. These results indicate a link between alterations in glycolytic metabolism and changes to Ca dynamics, two factors that have been implicated in neurodegeneration.
[Mh] Termos MeSH primário: Canais de Cálcio Tipo L/metabolismo
Cálcio/metabolismo
Cerebelo/patologia
Ativação do Canal Iônico
Neurônios/metabolismo
Deficiência de Tiamina/metabolismo
[Mh] Termos MeSH secundário: Animais
Animais Recém-Nascidos
Immunoblotting
Ratos Wistar
Período Refratário Eletrofisiológico
Deficiência de Tiamina/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Calcium Channels, L-Type); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:171018
[Lr] Data última revisão:
171018
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160504
[St] Status:MEDLINE
[do] DOI:10.1007/s10571-016-0378-8


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[PMID]:27040813
[Au] Autor:Matsukura S; Nakamura Y; Cao X; Wada T; Izumi-Nakaseko H; Ando K; Sugiyama A
[Ad] Endereço:Department of Pharmacology, Faculty of Medicine, Toho University, 5-21-16, Omori-nishi, Ota-ku, Tokyo, 143-8540, Japan.
[Ti] Título:Anti-atrial Fibrillatory Versus Proarrhythmic Potentials of Amiodarone: A New Protocol for Safety Evaluation In Vivo.
[So] Source:Cardiovasc Toxicol;17(2):157-162, 2017 Apr.
[Is] ISSN:1559-0259
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Anti-atrial fibrillatory and proarrhythmic potentials of amiodarone were simultaneously analyzed by using the halothane-anesthetized beagle dogs (n = 4) in order to begin to prepare standard protocol for clarifying both efficacy and adverse effects of anti-atrial fibrillatory drugs. Intravenous administration of 0.3 mg/kg of amiodarone hydrochloride decreased the heart rate and mean blood pressure. Additional administration of 3 mg/kg of amiodarone hydrochloride prolonged the QT interval besides the effects observed by the low dose, whereas it showed 1.6 times larger prolongation in the effective refractory period of the atrium than that of the ventricle, which may explain its clinical efficacy against atrial arrhythmias. However, no significant change was detected by either dose in the early repolarization assessed by corrected J-T or the late repolarization done by T -T in the electrocardiogram, although the former tended to be shortened and the reverse was true for the latter. Lack of prolongation in the early repolarization will make it feasible to better understand why amiodarone lacks proarrhythmic potential in spite of the QT-interval prolongation. Thus, these results of amiodarone obtained by current protocol may become a guidance on assessing efficacy and adverse effects of new anti-atrial fibrillatory drugs in vivo.
[Mh] Termos MeSH primário: Amiodarona/farmacologia
Antiarrítmicos/farmacologia
Antiarrítmicos/toxicidade
Fibrilação Atrial/tratamento farmacológico
Frequência Cardíaca/efeitos dos fármacos
[Mh] Termos MeSH secundário: Potenciais de Ação
Amiodarona/toxicidade
Animais
Fibrilação Atrial/diagnóstico
Fibrilação Atrial/fisiopatologia
Pressão Sanguínea/efeitos dos fármacos
Estimulação Cardíaca Artificial
Modelos Animais de Doenças
Cães
Relação Dose-Resposta a Droga
Eletrocardiografia
Feminino
Masculino
Período Refratário Eletrofisiológico
Medição de Risco
Fatores de Tempo
Torsades de Pointes/induzido quimicamente
Torsades de Pointes/fisiopatologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); N3RQ532IUT (Amiodarone)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171013
[Lr] Data última revisão:
171013
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160405
[St] Status:MEDLINE
[do] DOI:10.1007/s12012-016-9369-8



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