Electrophysiology

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Electrophysiology

  • atrial electrophysiology
  • cardiac electrophysiology
  • clinical electrophysiology
  • patch-clamp electrophysiology

  • Terms modified by Electrophysiology

  • electrophysiology laboratory
  • electrophysiology study

  • Selected Abstracts


    Journal of Cardiovascular Electrophysiology,2009

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2010
    Eric N. Prystowsky M.D.
    No abstract is available for this article. [source]


    Journal of Cardiovascular Electrophysiology , 2008

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2009
    Eric N. Prystowsky M.D.
    No abstract is available for this article. [source]


    Journal of Cardiovascular Electrophysiology , 2007

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2008
    Eric N. Prystowsky M.D.
    No abstract is available for this article. [source]


    Journal of Cardiovascular Electrophysiology,2006

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2007
    Eric N. Prystowsky M.D.
    No abstract is available for this article. [source]


    Journal of Cardiovascular Electrophysiology,2005

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 2 2006
    Eric N. Prystowsky M.D.
    No abstract is available for this article. [source]


    Basic Electrophysiology of the Pulmonary Veins and Their Role in Atrial Fibrillation:

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2003
    Perpetuators, Perplexers, Precipitators
    First page of article [source]


    International Consensus on Nomenclature and Classification of Atrial Fibrillation: A Collaborative Project of the Working Group on Arrhythmias and the Working Group of Cardiac Pacing of the European Society of Cardiology and the North American Society of Pacing and Electrophysiology

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2003
    SAMUEL LÉVY M.D.
    No abstract is available for this article. [source]


    Effects of Estrogen on Cardiac Electrophysiology in Female Mice

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 3 2002
    SAMIR SABA M.D.
    Estrogen and Cardiac Electrophysiology.Introduction: Understanding the molecular mechanisms that underlie gender- and hormonal-related differences in susceptibility to cardiac arrhythmias has been hampered by the lack of a suitable animal model. We examined the effect of hormonal status on the electrophysiologic (EP) properties of the mouse heart in an in vivo, closed chest model. Methods and Results: Fifty-three female C57/J mice aged 10 to 12 weeks were studied. Thirty-six mice underwent bilateral ovariectomies; 18 received estrogen (OVX + E) and 18 received placebo (OVX). Seventeen female mice underwent only sham surgery. All animals underwent in vivo EP studies. Select EP parameters were measured after quinidine treatment. Data were analyzed by a blinded observer. Compared with the intact female mice, the PR and AH intervals were significantly shorter in the OVX mice, and these parameters normalized with estrogen replacement (PR = 45.9 ± 4.5 msec in the intact mice, 42.1 ± 4.3 msec in the OVX group, and 46.9 ± 3.5 msec in the OVX + E group, P < 0.005; AH = 36.5 ± 4.9 msec in the intact mice, 34.4 ± 4.7 msec in the OVX group, and 38.8 ± 2.7 msec in the OVX + E group, P = 0.03). The right ventricular effective refractory period was significantly shorter in the OVX mice versus the intact mice, and this also normalized with estrogen replacement. Hormonal status did not significantly affect any other EP variable, including QT interval. Conclusion: In female mice, estrogen prolongs AV nodal conduction and the right ventricular effective refractory period. Taken together, these data suggest that hormonal status affects aspects of cardiac EP function. Future application of this mouse model will be helpful in determining the molecular pathways that mediate hormonal differences in cardiac EP. [source]


    Electrophysiology and Anatomic Characterization of an Epicardial Accessory Pathway

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 12 2001
    JOHN SAPP M.D.
    Epicardial Accessory Pathway. Pericardial access permitted epicardial catheter mapping and ablation of a rapidly conducting posteroseptal accessory pathway (AP) that had failed repeated ablation attempts. Transient block was achieved at the site of an AP potential. The AP was visible at surgery and resected. Histologic examination revealed cells typical of specialized cardiac conduction tissue. The location, size, and presence of conduction tissue likely account for failure of catheter ablation and resistance to drug therapy. [source]


    Consensus Statement from the Cardiac Nomenclature Study Group of Arrhythmias of the European Society of Cardiology, and the Task Force on Cardiac Nomenclature from the North American Society of Pacing and Electrophysiology on Living Anatomy of the Atrioventricular Junctions

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000
    DARLENE K. RACKER PH.D.
    [source]


    Consensus Statement from the Cardiac Nomenclature Study Group of Arrhythmias of the European Society of Cardiology, and the Task Force on Cardiac Nomenclature from the North American Society of Pacing and Electrophysiology on Living Anatomy of the Atrioventricular Junctions

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 11 2000
    Reply to the Editor
    [source]


    N -methyl-d-aspartate Receptor Responses Are Differentially Modulated by Noncompetitive Receptor Antagonists and Ethanol in Inbred Long-Sleep and Short-Sleep Mice: Behavior and Electrophysiology

    ALCOHOLISM, Issue 12 2000
    Taleen Hanania
    Background: Short-sleep (SS) mice exhibit higher locomotor activity than do long-sleep (LS) mice when injected with low doses of ethanol or the noncompetitive N -methyl-D-aspartate receptor (NMDAR) antagonist MK-801 (dizocilpine). SS mice also have higher densities of brain NMDARs. However, two strains of LS X SS recombinant inbred (RI) mice also show differential activation to ethanol and MK-801, but have similar numbers of NMDARs. Here we used inbred LS (ILS) and SS (ISS) mice to investigate further the relationship between NMDARs and sensitivity to the stimulant effects of low doses of ethanol. Methods: Open field activity and spontaneous alternations were measured after saline or drug injection. [3H]MK-801 binding parameters were determined in hippocampus, cortex, striatum, and nucleus accumbens. Extracellular field excitatory postsynaptic potentials (fEPSPs) were recorded in the CA1 region of hippocampal slices. Results: Systemic injection of either ethanol or MK-801 increased locomotor activity to a greater extent in ISS mice than in ILS mice. The competitive NMDAR antagonist 2-carboxypiperazin-4-yl-propyl-1,1phosphonic acid (±CPP) depressed activity of ILS, but not ISS, mice. No strain differences were observed in spontaneous alternations or in the number or affinity of NMDARs in the brain regions examined. Likewise, the magnitudes of hippocampal NMDAR-mediated fEPSPs were similar in ILS and ISS mice and were inhibited to the same extent by a competitive NMDAR antagonist. However, both ethanol and the NMDAR NR2B receptor antagonist ifenprodil inhibited the late component of hippocampal NMDAR fEPSPs to a greater extent in ISS, than in ILS, mice. Conclusions: Differential ethanol- and MK-801-induced behavioral activation in ILS and ISS mice was not associated with differences in NMDAR number. Nonetheless, pharmacological differences in hippocampal NMDAR responsiveness suggest that ISS mice express NMDARs that have a greater sensitivity to noncompetitive, but not competitive, NMDAR antagonists. These differences, which may reflect differences in NMDAR subunit composition, could underlie the differential responsiveness to low doses of ethanol in ILS and ISS mice. [source]


    Atrial, SA Nodal, and AV Nodal Electrophysiology in Standing Horses: Normal Findings and Electrophysiologic Effects of Quinidine and Diltiazem

    JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2007
    Colin C. Schwarzwald
    Background: Although atrial arrhythmias are clinically important in horses, atrial electrophysiology has been incompletely studied. Hypotheses: Standard electrophysiologic methods can be used to study drug effects in horses. Specifically, the effects of diltiazem on atrioventricular (AV) nodal conduction are rate-dependent and allow control of ventricular response rate during rapid atrial pacing in horses undergoing quinidine treatment. Animals: Fourteen healthy horses. Methods: Arterial blood pressure, surface electrocardiogram, and right atrial electrogram were recorded during sinus rhythm and during programmed electrical stimulation at baseline, after administration of quinidine gluconate (10 mg/kg IV over 30 minutes, n = 7; and 12 mg/kg IV over 5 minutes followed by 5 mg/kg/h constant rate infusion for the remaining duration of the study, n = 7), and after coadministration of diltiazem (0.125 mg/kg IV over 2 minutes repeated every 12 minutes to effect). Results: Quinidine significantly prolonged the atrial effective refractory period, shortened the functional refractory period (FRP) of the AV node, and increased the ventricular response rate during atrial pacing. Diltiazem increased the FRP, controlled ventricular rate in a rate-dependent manner, caused dose-dependent suppression of the sinoatrial node and produced a significant, but well tolerated decrease in blood pressure. Effective doses of diltiazem ranged from 0.125 to 1.125 mg/kg. Conclusions and Clinical Importance: Standard electrophysiologic techniques allow characterization of drug effects in standing horses. Diltiazem is effective for ventricular rate control in this pacing model of supraventricular tachycardia. The use of diltiazem for rate control in horses with atrial fibrillation merits further investigation. [source]


    Cavotricuspid Isthmus: Anatomy, Electrophysiology, and Long-Term Outcome of Radiofrequency Ablation

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 12 2009
    Ching-Tai Tai M.D.
    The cavotricuspid isthmus (CTI) had a complex architecture with an anisotropic conduction property. An incremental pacing from the low right atrial isthmus produced a conduction delay and block, and initiated atrial flutter. Radiofrequency catheter ablation of the CTI was very effective in eliminating the typical atrial flutter. However, atrial fibrillation often occurred after ablation of the isthmus and needs further treatment. [source]


    The Twelfth World Symposium of Cardiac Pacing and Electrophysiology

    PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p1 2003
    SEYMOUR FURMAN
    No abstract is available for this article. [source]


    Electrosurgery after Cochlear Implantation: Eighth Nerve Electrophysiology,

    THE LARYNGOSCOPE, Issue 12 2004
    David M. Poetker MD
    Abstract Hypothesis: Monopolar electrosurgery below the neck in cochlear implant recipients can be performed without damage to the internal cochlear stimulator, electrode array, and the cochlear nerve. Study Design: Prospective pre- and postintervention electrically evoked compound action potential (ECAP) study of cochlear nerve function and behavioral sound perception assessment. Methods: Neural response telemetry (NRT) was used to measure ECAPs before and after the use of monopolar electrosurgery during coronary artery bypass surgery to assess prosthetic device function and electrophysiologic function of the cochlear nerve. In addition, electrode voltage impedances and behavioral sound perception was measured at the same time intervals. Results: ECAPs, behavioral sound perception, and electrode voltage impedances were within the normal range, within compliance, and similar preoperatively and on postoperative day 6. Conclusion: The studies reported herein were a series of measurements designed to test neural integrity and prosthetic device function before and after the use of monopolar electrosurgery. With appropriate precautions, use of monopolar electrosurgery below the neck in cochlear implant recipients can be performed safely. [source]


    Antiprogesterone therapy uncouples axonal loss from demyelination in a transgenic rat model of CMT1A neuropathy

    ANNALS OF NEUROLOGY, Issue 1 2007
    Gerd Meyer zu Horste MD
    Objective Charcot,Marie,Tooth disease (CMT) is the most common inherited neuropathy, and a duplication of the Pmp22 gene causes the most frequent subform CMT1A. Using a transgenic rat model of CMT1A, we tested the hypothesis that long-term treatment with anti-progesterone (Onapristone) reduces Pmp22 overexpression and improves CMT disease phenotype of older animals, thereby extending a previous proof-of-concept observation in a more clinically relevant setting. Methods We applied placebo-controlled progesterone-antagonist therapy to CMT rats for 5 months and performed grip-strength analysis to assess the motor phenotype. Quantitative Pmp22 RT-PCR and complete histological analysis of peripheral nerves and skin biopsies were performed. Results Anti-progesterone therapy significantly increased muscle strength and muscle mass of CMT rats and reduced the performance difference to wildtype rats by about 50%. Physical improvements can be explained by the prevention of axon loss. Surprisingly, the effects of anti-progesterone were not reflected by improved myelin sheath thickness. Electrophysiology confirmed unaltered NCV, but less reduced CMAP recordings in the treatment group. Moreover, the reduction of Pmp22 mRNA, as quantified in cutaneous nerves, correlated with the clinical phenotype at later stages. Interpretation Progesterone-antagonist treatment. Pmp22 overexpression to a degree at which the axonal support function of Schwann cells is better maintained than myelination. This suggests that axonal loss in CMT1A is not caused by demyelination, but rather by a Schwann cell defect that has been partially uncoupled by anti-progesterone treatment. Pmp22 expression analysis in skin may provide a prognostic marker for disease severity and for monitoring future clinical trials. Ann Neurol 2007;61:61,72 [source]


    Correlation of Noninvasive Electrocardiography with Invasive Electrophysiology in Syncope of Unknown Origin: Implications from a Large Syncope Database

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009
    Konstantinos A. Gatzoulis
    Background: The evaluation of syncope can be expensive, unfocussed, and unrevealing yet, failure to diagnose an arrhythmic cause of syncope is a major problem. We investigate the utility of noninvasive electrocardiographic evaluation (12-lead ECG and 24-hour ambulatory electrocardiographic recordings) to predict electrophysiology study results in patients with undiagnosed syncope. Methods: We evaluated 421 patients with undiagnosed syncope who had an electrocardiogram (ECG), an electrophysiology study, and 24-hour ambulatory monitoring. Noninvasive testing was used to predict electrophysiology testing outcomes. Multivariable logistic regression analysis adjusting for age, sex, presence of heart disease, and left ventricular ejection fraction (LVEF) was used to assess independent predictors for sinus node disease, atrioventricular node disease, and induction of ventricular tachyarrhythmias. Results: Patients were divided into four groups: group 1, abnormal ECG and ambulatory monitor; group 2, abnormal ECG only; group 3, abnormal ambulatory monitor; and group 4, normal ECG and ambulatory monitor. The likelihood of finding at least one abnormality during electrophysiologic testing among the four groups was highest in group 1 (82.2%) and lower in groups 2 and 3 (68.1% and 33.7%, respectively). In group 4, any electrophysiology study abnormality was low (9.1%). Odds ratios (OR) were 35.9 (P < 0.001), 17.8 (P < 0.001), and 3.5 (P = 0.064) for abnormal findings on electrophysiology study, respectively (first three groups vs the fourth one). ECG and ambulatory monitor results predicted results of electrophysiology testing. Conclusion: Abnormal ECG findings on noninvasive testing are well correlated with potential brady- or/and tachyarrhythmic causes of syncope, in electrophysiology study of patients with undiagnosed syncope. [source]


    Pilot Study: Noninvasive Monitoring of Oral Flecainide's Effects on Atrial Electrophysiology during Persistent Human Atrial Fibrillation Using the Surface Electrocardiogram

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2005
    Daniela Husser M.D.
    Background: The relation between flecainide's plasma level and its influence on human atrial electrophysiology during acute and maintenance therapy of atrial fibrillation (AF) is unknown. Therefore, this study determined flecainide plasma levels and atrial fibrillatory rate obtained from the surface ECG during initiation and early maintenance of oral flecainide in patients with persistent lone AF and assessed their relationship. Methods and Results: In 10 patients (5 males, mean age 63 ± 14 years, left atrial diameter 46 ± 3 mm) with persistent lone AF, flecainide was administered as a single oral bolus (day 1) followed by 200,400 mg/day (days 2,5). The initial 300 mg flecainide bolus resulted in therapeutic plasma levels in all patients (range 288,629 ng/ml) with no side effects. Flecainide plasma levels increased on day 3 and remained stable thereafter. Day 5 plasma levels were lower (508 ± 135 vs 974 ± 276 ng/ml, P = 0.009) in patients with daily mean flecainide doses of 200 mg compared to patients with higher maintenance doses. Fibrillatory rate obtained from the surface electrocardiogram measuring 378 ± 17 fpm at baseline was reduced to 270 ± 18 fpm (P < 0.001) after the flecainide bolus but remained stable thereafter. Fibrillatory rate reduction was independent of flecainide plasma levels or clinical variables. Conclusion: A 300 mg oral flecainide bolus is associated with electrophysiologic effects that are not increased during early maintenance therapy in persistent human lone AF. In contrast to drug plasma levels, serial analysis of fibrillatory rate allows monitoring of individual drug effects on atrial electrophysiology. [source]


    Electrophysiology and Hemodynamics of Open Chest Resuscitation from Cardiac Arrest in a Swine

    ACADEMIC EMERGENCY MEDICINE, Issue 1 2009
    Bphil, David D. Salcido BS
    First page of article [source]


    4341: Are visual evoked potentials and pattern ERG useful in neuro-ophthalmology?

    ACTA OPHTHALMOLOGICA, Issue 2010
    GE HOLDER
    Purpose To describe the roles of VEP and PERG in clinical neuroophthalmology. Methods Case based examples. Results Objective visual system testing with electrophysiology allows the distinction between optic nerve and macular dysfunction, often difficult in clinical practice. Examples will be shown of the types of VEP abnormality that can occur in different disorders of optic nerve function. PERG should also be performed in the patient with visual symptoms; if the PERG suggests macular dysfunction, full-field ERG is indicated in order to determine whether that macular dysfunction is part of a generalised retinal process or is dysfunction localised to the macula. Electrophysiology further allows the diagnosis of non-organic visual loss and the quantification of visual system dysfunction. Conclusion The objective functional assessment with electrophysiology is an important part of the diagnostic armamentarium available to neuroophthalmologists. [source]


    2245: Electrodiagnosis in inherited retinal disease

    ACTA OPHTHALMOLOGICA, Issue 2010
    GE HOLDER
    Purpose To describe the roles of electrophysiology in the diagnosis and counselling of patients with inherited retinal disease. Methods Electrophysiological testing performed to incorporate and extend the recommendations of the International Society for Clinical Electrophysiology of Vision. Results Using a case-based presentation, it will be shown that electrophysiological testing can objectively assess the function of the different cell types and layers within the retina of the patient with inherited retinal dysfunction, which enables accurate diagnosis and counselling when placed in clinical context. The roles of pattern and multi-focal ERG in the assessment of macular function will be discussed. The electrophysiological findings will be discussed in relation to imaging studies when appropriate. It will shown that distinctive electrophysiological findings can direct appropriate and therefore cost-effective mutational screening in patients with atypical fundus changes. Conclusion Electrophysiological testing is fundamental to the successful management of patients with inherited disorders of retinal function. [source]


    4124: Electrophysiology of childhood retinal dystrophies

    ACTA OPHTHALMOLOGICA, Issue 2010
    M BROWN
    Purpose To provide a systematic approach to the diagnosis of causes of impaired vision in childhood with particular reference to the role of electrophysiology in retinal dystrophies Methods We have examined the contribution Electrodiagnostic Testing (EDT) can make in determining or confirming a diagnosis. Results We have set out a systematic approach to diagnosis of both early and late onset disorders, differentiating between retinal and non-retinal causes. Signs, symptoms, inheritance patterns and test results are tabulated against specific disorders showing the contribution EDT can make. Recent example case studies are also presented. Conclusion Electrodiagnostic testing is of particular value in identifying and differentiating causes of poor vision where there may not be clear retinal signs in the early stages such as Leber's congenital amaurosis, CSNB, cone dystrophy and albinism. A further role is in the differentiation of retinal from post-retinal causes. [source]


    Is AZOOR an autoimmune disease?

    ACTA OPHTHALMOLOGICA, Issue 2007
    SF SEIDOVA
    Purpose: Acute zonal occult outer retinopathy (AZOOR) is one of the "white dot syndromes" a clinically heterogeneous group of inflammatory chorioretinopathies. The etiology is not yet clear. Methods: We present a 50 years female patient with a prior history of migraine. She experienced progressive visual loss and visual field defects in the last 3 years. Preceding each episode she experienced blue flickering photopsias. Results: Visual acuity was 0,3 in the right eye and 0,6 in the left eye. Biomicroscopy showed a normal anterior segment, fundus exam revealed pigment epithelial atrophy more pronounced in the worse eye. Electrophysiology showed a marked reduction in the photopic ERG in the more affected eye. MRI demonstrated multiple white matter lesions including a corpus callosum location. Lumbar puncture showed oligoclonal bands. Further tests demonstrated hearing impairment. Therapy was instituted during the three years course of the disease with steroids, immune suppressants and plasmapheresis with visual loss being progressive. New photopsia is currently present. Conclusions: The etiology of AZOOR remains unclear. With our patient being one of the few described in the literature with concomitant multiple sclerosis, the question remains on whether there is an underlying common process of inflammatory autoimmune reactions. Whether treatment is possible, remains to be evaluated. [source]


    The key role of electrophysiology in the diagnosis of visually impaired children

    ACTA OPHTHALMOLOGICA, Issue 6 2006
    Maria Van Genderen
    Abstract. Purpose:, To describe the outcome of specialized electrophysiology in visually impaired children. Methods:, We carried out a retrospective evaluation of 340 electrophysiological examinations performed in 298 children over a 3-year period (2001,2003), with regard to demographic data, referral pattern, degree of compliance, and diagnostic results. Electrophysiology was performed without sedation or anaesthesia. In electroretinograms, DTL electrodes were used in combination with online selection of responses. Visual evoked potentials testing was performed with seven active occipital electrodes. Results:, The mean age of the children was 7 ± 5 years; 72 (24%) of the children were mentally as well as visually impaired. Main reasons for referral were suspected posterior segment disease, abnormal visual development, unexplained low vision, high myopia, and suspected albinism. Compliance was good in 302/340 (88%), partial in 24/340 (7%), and absent in 14/340 (4%) of the examinations. Of the 326 successful procedures, 215 (66%) showed abnormal results. Tapetoretinal dystrophy (22%), opticopathy (16%), congenital stationary night blindness (13%), and cone dystrophy (11%) were the most frequently established diagnoses. Albinism was confirmed in 14 of 24 suspected patients; additionally, unsuspected misrouting was found in six. In 26 (9%) of the patients, a previously established diagnosis was changed. Conclusions:, In a specialized setting, electrophysiological examinations can be performed successfully in visually impaired children. The results are essential for the final ophthalmological diagnosis and have important consequences for rehabilitation. [source]


    c-Kit+ Bone Marrow Stem Cells Differentiate into Functional Cardiac Myocytes

    CLINICAL AND TRANSLATIONAL SCIENCE, Issue 1 2009
    Hajime Kubo Ph.D.
    Abstract The utility of bone marrow cells (BMCs) to regenerate cardiac myocytes is controversial. The present study examined the capacity of different types of BMCs to generate functional cardiac myocytes. Isolated c-kit+ BMCs (BMSCs), c-kit+ and crude BMCs from the adult feline femur were membrane stained with PKH26 dye or infected with a control enhanced green fluorescence protein transcript (EGFP)-adenovirus prior to co-culture upon neonatal rat ventricular myocytes (NRVM). Co-cultured cells were immuno-stained for c-kit, ,-tropomyosin, ,-actinin, connexin 43 (C×43) and Ki67 and analyzed with confocal microscopy. Electrophysiology of BMSC derived myocytes were compared to NRVMs within the same culture dish. Gap junction function was analyzed by fluorescence recovery after photo-bleaching (FRAP). BMCs proliferated and differentiated into cardiac myocytes during the first 48 hours of co-culturing. These newly formed cardiac myocytes were able to contract spontaneously or synchronously with neighboring NRVMs. The myogenic rate of c-kit+ BMSCs was significantly greater than c-kit+ and crude BMCs (41.2 ± 2.1, 6.1 ± 1.2, and 17.1 ± 1.5%, respectively). The newly formed cardiac myocytes exhibited an immature electrophysiological phenotype until they became electrically coupled to NRVMs through functional gap junctions. BMSCs did not become functional myocytes in the absence of NRVMs. In conclusion, c-kit+ BMSCs have the ability to transdifferentiate into functional cardiac myocytes. [source]


    Rhythm Management in Pediatric Heart Failure

    CONGENITAL HEART DISEASE, Issue 4 2006
    Charles I. Berul MD
    ABSTRACT There are several options now available for the management of arrhythmias and ventricular dysfunction in pediatric patients with heart failure. A hybrid approach that combines the expertise of heart failure and electrophysiology specialists may be well suited for the optimal management of these complex patients. Medical and device therapies may be synergistic in decreasing the morbidity and mortality in pediatric heart failure. Pediatric electrophysiology can now potentially offer therapies that can help prevent both arrhythmic and pump failure deaths, as well as improve functional capacity and quality of life. These therapies and the available supporting data relevant to pediatrics will be the focus of this review. [source]


    Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties

    ACTA PHYSIOLOGICA, Issue 1 2010
    P. Hakim
    Abstract Aim:, In contrast to extensive reports on the roles of Nav1.5 , -subunits, there have been few studies associating the , -subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b,/, mice. Methods:, The following properties were compared in the hearts of wild-type (WT) and Scn3b,/, mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the ,3 protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts. Results:,Scn3b mRNA was expressed in the atria of WT but not Scn3b,/, hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the ,3 protein was expressed in WT and absent in Scn3b,/, cardiac myocytes. Lead I electrocardiograms from Scn3b,/, mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b,/, hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b,/, but hardly any WT hearts. Scn3b,/, hearts also demonstrated significantly longer sinus node recovery times than WT hearts. Conclusion:, These findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion. [source]


    The role of inhibitory neurotransmission in locomotor circuits of the developing mammalian spinal cord

    ACTA PHYSIOLOGICA, Issue 2 2009
    H. Nishimaru
    Abstract Neuronal circuits generating the basic coordinated limb movements during walking of terrestrial mammals are localized in the spinal cord. In these neuronal circuits, called central pattern generators (CPGs), inhibitory synaptic transmission plays a crucial part. Inhibitory synaptic transmission mediated by glycine and GABA is thought to be essential in coordinated activation of muscles during locomotion, in particular, controlling temporal and spatial activation patterns of muscles of each joint of each limb on the left and right side of the body. Inhibition is involved in other aspects of locomotion such as control of speed and stability of the rhythm. However, the precise roles of neurotransmitters and their receptors mediating inhibitory synaptic transmission in mammalian spinal CPGs remain unclear. Moreover, many of the inhibitory interneurones essential for output pattern of the CPG are yet to be identified. In this review, recent advances on these issues, mainly from studies in the developing rodent spinal cord utilizing electrophysiology, molecular and genetic approaches are discussed. [source]


    Attention-like processes underlying optomotor performance in a Drosophila choice maze

    DEVELOPMENTAL NEUROBIOLOGY, Issue 2 2007
    Bruno van Swinderen
    Abstract The authors present a novel paradigm for studying visual responses in Drosophila. An eight-level choice maze was found to reliably segregate fly populations according to their responses to moving stripes displayed on a computer screen. Visual responsiveness was robust in wild-type flies, and performance depended on salience effects such as stimulus color and speed. Analysis of individual fly choices in the maze revealed that stereotypy, or choice persistence, contributed significantly to a strain's performance. On the basis of these observations, the authors bred wild-type flies for divergent visual phenotypes by selecting individual flies displaying extreme stereotypy. Selected flies alternated less often in the sequential choice maze than unselected flies, showing that stereotypy could evolve across generations. The authors found that selection for increased stereotypy impaired flies' responsiveness to competing stimuli in tests for attention-like behavior in the maze. Visual selective attention was further investigated by electrophysiology, and it was found that increased stereotypy also impaired responsiveness to competing stimuli at the level of brain activity. Combined results present a comprehensive approach to studying visual responses in Drosophila, and show that behavioral performance involves attention-like processes that are variable among individuals and thus sensitive to artificial selection. © 2006 Wiley Periodicals, Inc. Develop Neurobiol 67: 129,145, 2007. [source]