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We present the first long-duration and high duty cycle 40-T pulsed-field cryomagnet addressed to single crystal neutron diffraction experiments at temperatures down to 2 K. The magnet produces a horizontal field in a bi-conical geometry, ±15° and ±30° upstream and downstream of the sample, respectively. Using a 1.15 MJ mobile generator, magnetic field pulses of 100 ms length are generated in the magnet, with a rise time of 23 ms and a repetition rate of 6-7 pulses per hour at 40 T. The setup was validated for neutron diffraction on the CEA-CRG three-axis spectrometer IN22 at the Institut Laue Langevin.

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URu2Si2 is one of the most enigmatic strongly correlated electron systems and offers a fertile testing ground for new concepts in condensed matter science. In spite of >30 years of intense research, no consensus on the order parameter of its low-temperature hidden-order phase exists. A strong magnetic field transforms the hidden order into magnetically ordered phases, whose order parameter has also been defying experimental observation. Here, thanks to neutron diffraction under pulsed magnetic fields up to 40 T, we identify the field-induced phases of URu2Si2 as a spin-density-wave state. The transition to the spin-density wave represents a unique touchstone for understanding the hidden-order phase. An intimate relationship between this magnetic structure, the magnetic fluctuations and the Fermi surface is emphasized, calling for dedicated band-structure calculations.

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Although bipolar jets are seen emerging from a wide variety of astrophysical systems, the issue of their formation and morphology beyond their launching is still under study. Our scaled laboratory experiments, representative of young stellar object outflows, reveal that stable and narrow collimation of the entire flow can result from the presence of a poloidal magnetic field whose strength is consistent with observations. The laboratory plasma becomes focused with an interior cavity. This gives rise to a standing conical shock from which the jet emerges. Following simulations of the process at the full astrophysical scale, we conclude that it can also explain recently discovered x-ray emission features observed in low-density regions at the base of protostellar jets, such as the well-studied jet HH 154.

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We have developed a pulsed magnet system with panoramic access for synchrotron x-ray diffraction in magnetic fields up to 31 T and at low temperature down to 1.5 K. The apparatus consists of a split-pair magnet, a liquid nitrogen bath to cool the pulsed coil, and a helium cryostat allowing sample temperatures from 1.5 up to 250 K. Using a 1.15 MJ mobile generator, magnetic field pulses of 60 ms length were generated in the magnet, with a rise time of 16.5 ms and a repetition rate of 2 pulses/h at 31 T. The setup was validated for single crystal diffraction on the ESRF beamline ID06.

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The production of strongly magnetized laser plasmas, of interest for laboratory astrophysics and inertial confinement fusion studies, is presented. This is achieved by coupling a 16 kV pulse-power system. This is achieved by coupling a 16 kV pulse-power system, which generates a magnetic field by means of a split coil, with the ELFIE laser facility at Ecole Polytechnique. In order to influence the plasma dynamics in a significant manner, the system can generate, repetitively and without debris, high amplitude magnetic fields (40 T) in a manner compatible with a high-energy laser environment. A description of the system and preliminary results demonstrating the possibility to magnetically collimate plasma jets are given.

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We report on the design, construction, and operation of a horizontal field, 30 T magnet system with a conical bore optimized for synchrotron x-ray powder diffraction. The magnet offers ±31° optical access downstream of the sample, which allows to measure a sufficiently large number of Debye rings for an accurate crystal structure analysis. Combined with a 290 kJ generator, magnetic field pulses of 60 ms length were generated in the magnet, with a rise time of 4.1 ms and a repetition rate of 6 pulses/h at 30 T. The coil is mounted inside a liquid nitrogen bath. A liquid helium flow cryostat reaches into the coil and allows sample temperature between 5 and 250 K. The setup was used on the European Synchrotron Radiation Facility beamlines ID20 and ID06.

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INTRODUCTION: The properties and substrates of slow and fast AV nodal pathway remain unclear. This applies particularly to the slow pathway (SP), which is largely concealed by fast pathway (FP) conduction. We designed a new FP ablation approach that exposes the SP over the entire cycle length range and allows for its independent characterization and ablation. METHODS AND RESULTS: Premature stimulation was performed before and after FP ablation with 5.4 +/- 1.9 lesions (300-microm diameter each; overall lesion size 1.4 +/- 0.5 mm) targeting the junction between perinodal and compact node tissues in seven rabbit heart preparations. The resulting SP recovery curve and control curve had the same maximum nodal conduction time (165 +/- 22 msec vs 164 +/- 24 msec; P = NS) and effective refractory period (101 +/- 10 msec vs 100 +/- 9 msec; P = NS). The two curves covered the same cycle length range. However, the SP curve was shifted up with respect to control one at intermediate and long cycle lengths and thus showed a longer minimum nodal conduction time (81 +/- 15 msec vs 66 +/- 10 msec; P < 0.01) and functional refractory period (180 +/- 11 msec vs 170 +/- 12 msec; P < 0.05). The SP curve was continuous and closely fitted by a single exponential function. Small local lesions (2 +/- 1) applied to the posterior nodal extension resulted in third-degree nodal block in all preparations. CONCLUSION: The posterior nodal extension can sustain effective atrial-His conduction at all cycle lengths and account for both the manifest and concealed portion of SP. Slow and FP conduction primarily arise from the posterior extension and compact node, respectively.

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INTRODUCTION: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. METHODS AND RESULTS: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (approximately 300 microm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 +/- 16 ms to 123 +/- 11 msec (P < 0.01) and prolonged the effective refractory period from 104 +/- 6 msec to 119 +/- 11 msec (P < 0.01) without affecting A2H2min (55 +/- 9 msec vs 55 +/- 8 msec; P = NS) and functional refractory period (174 +/- 7 msec vs 175 +/- 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. CONCLUSION: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.

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INTRODUCTION: The circuitry underlying AV nodal reentry remains debated. We developed a model of AV nodal reentry and assessed the role of nodal inputs, compact node, and its posterior nodal extension (PNE) in this phenomenon. METHODS AND RESULTS: A fine scanning of short coupling interval range with an atrial premature beat consistently initiated slow-fast AV nodal reentrant beats that occurred 37+/-31 msec (mean+/-SD) after His-bundle activation in 11 of 16 consecutive rabbit heart preparations. The repeated testing (>40 times) of a chosen coupling interval within reentry window (6+/-9 msec, n = 11) yielded reentrant intervals that varied by 2+/-1 msec (mean SD for 40 beats+/-SD, n = 11). The breakthrough point of reentrant activation, as assessed from four perinodal sites, varied in different preparations from diffuse (4) to anterior (1), medial (3), or posterior (3); mean reentrant interval did not differ between perinodal sites. Antegrade perinodal activation pattern did not differ at reentrant versus nonreentrant coupling intervals and thus was not a primary determinant of reentry. A PNE ablation (n = 4) interrupted the slow pathway conduction and prevented reentry without affecting antegrade perinodal activation or fast pathway conduction. CONCLUSION: A reproducible model of AV nodal reentrant beats was developed and used to study underlying circuitry. The AV nodal reentry involves unaltered antegrade perinodal activation, slow PNE conduction and retrograde broad invasion of perinodal tissues starting at a preparation-dependent breakthrough point. A PNE ablation abolishes the reentry.

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BACKGROUND: The AV node is frequently the site of reentrant rhythms. These rhythms arise from a slow and a fast pathway for which the anatomic and functional substratum remain debated. This study proposes a new explanation for dual-pathway physiology in which the posterior nodal extension (PNE) provides the substratum for the slow pathway. METHODS AND RESULTS: The anatomic and functional properties of the PNE were studied in 14 isolated rabbit heart preparations. A PNE was found in all studied preparations. It appeared as an elongated bundle of specialized tissues lying along the lower side of Koch's triangle between the coronary sinus ostium and compact node. No well-defined boundary separated the PNE, compact node, and lower nodal cell bundle. The electric properties of the PNE were characterized with a premature protocol and surface potential recordings from histologically controlled locations. The PNE showed cycle-length-dependent posteroanterior slow activation with a shorter refractory period (minimum local cycle length) than that of the compact node. During early premature beats resulting in block in transitional tissues, the markedly delayed PNE activation could propagate to maintain or resume nodal conduction and initiate reentrant beats. A shift to PNE conduction resulted in different patterns of discontinuity on conduction curves. Transmembrane action potentials recorded from PNE cells in 6 other preparations confirmed the slow nature of PNE potentials. CONCLUSIONS: The PNE is a normal anatomic feature of the rabbit AV node. It constitutes a cycle-length-dependent slow pathway with a shorter refractory period than that of the compact node. Propagated PNE activation can account for a discontinuity in conduction curves, markedly delayed AV nodal responses, and reentry. Finally, the PNE provides a substratum for the slow pathway in dual-pathway physiology.

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INTRODUCTION: Alternation of atrial cycle length and AV nodal conduction time (NCT) is often observed during AV reentrant tachycardia. Both AV nodal dual pathway and rate-dependent function have been postulated to be involved in this phenomenon. This study was designed to determine the respective role of these two mechanisms in the alternation observed in an in vitro model of orthodromic AV reentrant tachycardia. METHODS AND RESULTS: The tachycardia was produced by detecting each His-bundle activation and stimulating the atrium after a retrograde delay, thereby simulating retrograde pathway conduction, in six isolated rabbit heart preparations. After a 5-minute stabilization period at a fast rate, the retrograde delay was decremented by 2 msec every minute until nodal blocks occurred. We observed a sequential alternation of the cycle length and NCT in four preparations in the short retrograde delay range. The magnitude of the alternation gradually increased as the retrograde delay was decreased and reached 4.6 +/- 0.5 msec during 1:1 conduction. The alternation increased further just prior to termination of the tachycardia by an AV nodal block. None of the preparations showed discontinuous AV nodal recovery curves. Moreover, an electrode positioned over the endocardial surface of the node showed that the alternation developed distally to the nodal inputs, which are believed to constitute a major component of dual pathways. A mathematical model predicted the alternation from known characteristics of rate-dependent nodal functional properties. CONCLUSIONS: NCT and cycle length alternation can arise during orthodromic AV reentrant tachycardia when the retrograde delay is sufficiently short. The characteristics of the alternation, presence of continuous recovery curves, intranodal location of the alternation, and mathematical modeling suggest that the alternation is predictable from the known functional properties of the AV node without postulating dual pathway physiology.

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BACKGROUND: The atrioventricular node receives its activation signal from the low crista terminalis and low interatrial septum, the summation of which is believed to favor conduction. A functional asymmetry between the inputs is also believed to be involved in nodal reentrant rhythms. We studied the selective functional characteristics of nodal inputs and determined their role in nodal conduction, refractoriness, summation, and rate-dependent function. METHODS AND RESULTS: The nodal properties of recovery, facilitation, and fatigue were characterized with stimulation protocols applied with varying phases between the two inputs in isolated rabbit heart preparations. The effects of the input phase, nodal functional state, and input reference on the nodal conduction time, recovery time, and refractory periods were assessed with multifactorial ANOVAs. It was found that the phase of stimulation significantly affected nodal conduction time but not the refractory periods or the time constant of the recovery. Each input could show longer and shorter conduction time than the other depending on the stimulation phase, input reference, and coupling interval. These effects were similar for different nodal functional states. However, pacing and recording from the low crista resulted in similar conduction and refractory values than did pacing and recording from the low septum. Input summation did not increase the otherwise equal efficacy of individual input in activating the node. Nodal surface recordings confirmed this functional symmetry and equivalent efficacy of the inputs and showed that input effects were confined to the proximal node. CONCLUSIONS: The two nodal inputs have equivalent functional properties and are equally effective in activating the rate-dependent portion of the node. Input interaction affects perinodal activation but not the rate-dependent nodal function.

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The characteristics and functional origin of the changes in transient atrioventricular (AV) nodal responses with heart rate history were studied in isolated rabbit heart preparations. For this purpose, ramp stimulation sequences were applied to the atrium from different initial conditions. A ramp decrease and increase in the His-stimulus interval and a reverse sequence consisting of a ramp increase and decrease were performed starting from a control basic cycle length, after 5 min of fast rate, or with 5 min of fast rate inserted between the two ramps. The nodal conduction times (NCT) obtained during the ramp stimulations formed hysteresis loops, the direction, shape, and magnitude of which varied markedly with the nodal history. That is, the nodal response to a given ramp took a variety of forms, depending on the initial condition. The effects of the initial condition also depended on ramp direction and sequence. A paradoxical NCT-recovery relationship (decrease in NCT with shortening His-atrial interval) was consistently observed at the onset of any ramp decrease performed after 5 min of fast rate. These effects also varied with the rate used to change the nodal history. The insertion of a control cycle at every 20th beat during repeated ramp protocols allowed the determination of the contribution of the nodal property of fatigue to these effects. Fatigue was found to account for all observed hysteresis patterns. In conclusion, heart rate history can, by modulating beat-to-beat changes in fatigue, transform transient nodal responses and hysteresis observed during stimulation ramps. Interpretation of transient nodal responses thus requires exact knowledge of previous nodal history.

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The functional origin of atrioventricular nodal hysteresis was studied in isolated rabbit heart preparations. This hysteresis is characterized by asymmetric changes in nodal conduction time (NCT) occurring for symmetric changes in cycle length. The respective contribution of the nodal properties of recovery, facilitation, and fatigue to the beat-to-beat changes in NCT observed during paired symmetric ramps of decreasing and increasing cycle length was determined with specifically design stimulation protocols. Nodal hysteresis was found to be entirely accounted for by variations in the contribution of nodal recovery and fatigue properties observed at corresponding cycle lengths. The study establishes how this contribution varies on a beat-to-beat basis as a result of cycle length history. This holds true for the numerous changes in hysteresis observed in response to changes in the sequence and slope of the ramps. Facilitation clearly affected NCT during these responses but did not contribute to the hysteresis. Moreover, the study demonstrates that there is no inherent change in the characteristics of nodal function with the direction of the ramp that could account for the hysteresis. Thus nodal hysteresis arises from nodal functional properties of recovery and fatigue but does not constitute a distinct independent intrinsic property of the node.

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The functional origin of the changes in atrioventricular (AV) nodal function with the atrial pacing site was studied in isolated rabbit heart preparations. The rate-dependent AV nodal properties of recovery, facilitation, and fatigue were characterized with premature stimulation protocols repeated for each of three atrial pacing sites (upper atrium, low crista terminalis, and low interatrial septum). The effects of the atrial pacing site, reference site from which the beginning of nodal activation is measured (low crista and low septum) and stimulation protocol on nodal conduction and refractory parameters, were assessed with multifactorial analyses of variance. The changes in nodal parameters with the stimulation protocol did not differ significantly with the pacing site, indicating that the rate-dependent nodal properties are not affected by the atrial origin of the impulse. Only the baseline value of nodal parameters varied with the atrial pacing and reference site. However, the comparison of data obtained while the low crista was the pacing and reference site to those obtained while the low septum was the pacing and reference site yield no statistically significant differences, thus indicating that changes in perinodal activation were largely responsible for the observed changes in baseline. Upper atrial and low crista pacing yielded very similar data. We conclude that 1) the atrial pacing site affects perinodal activation but not rate-dependent nodal function, 2) the two inputs are equally effective in activating the AV node, and 3) input summation is a minor factor in rate-dependent nodal function.

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A theoretical model, formulated as a finite difference equation is proposed for rate-dependent conduction properties of the atrioventricular (AV) node. The AV nodal conduction time, which is defined as the time interval from the atrial activation to the activation of the bundle of His, depends on the history of activation of the node. The theoretical model, which incorporates physiological concepts of recovery, facilitation and fatigue, accurately predicts a variety of experimentally observed complex rhythms of nodal conduction. In particular, alternans rhythms, in which there is an alternation in conduction time from beat to beat, are associated with period-doubling bifurcations in the theoretical model.

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INTRODUCTION: The rate-dependent changes in atrioventricular (AV) nodal conduction time show different characteristics depending upon whether the conduction times are plotted against the atrial interval (AA-recovery curve) or His-atrial interval (HA-recovery curve). This study characterizes these differences in the context of controlled changes of nodal functional properties, determines their functional significance, and tests the hypothesis that they are related solely to the nodal conduction time of the last beat (last conduction time) before the premature beat. METHODS AND RESULTS: Premature nodal conduction times obtained in isolated rabbit heart preparations under various steady-state and transient conditions were plotted as a function of the corresponding HA and AA intervals, as well as the AA interval corrected for the last conduction time. Under all conditions, the corrected AA-recovery curve was indistinguishable in shape from the HA-recovery curve, and as such reflected similar underlying nodal functional properties. Moreover, a selective increase in the last conduction time, induced in the absence of time-dependent effects associated with the functional property of fatigue, shifted the AA-recovery but not the HA-recovery curve upward with respect to the control curve. CONCLUSION: The last conduction time accounts entirely for differences between AA-recovery and HA-recovery curves that otherwise reflect the same underlying nodal functional state. Thus, a consistent assessment of rate-dependent changes in nodal function can be achieved with either measure of recovery time.

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The wide variety of delays that the atrioventricular node can generate in response to an increased rate are explained by dynamic interactions between the three intrinsic properties of recovery, facilitation, and fatigue. The functional model presented suggests that any deviation of nodal conduction time from its minimum basal value represents, at any given time, the net sum of the effects produced by these properties. When a constant fast atrial rate is suddenly initiated, the node first "sees" a shortening in recovery time and responds by an increase in conduction time. This increase further shortens the recovery time of the ensuing beat, which is accordingly further delayed, and so on until a steady state is reached or a block occurs. However, these events do not occur alone. The second beat at the fast rate is conducted with a shorter conduction time than expected from the recovery time alone, and is therefore facilitated. These facilitatory effects develop within one short cycle and dissipate within one long cycle. They affect increasingly the conduction time of beats occurring with shorter cycle lengths. While steady-state effects of recovery and facilitation occur within seconds, nodal conduction time continues to increase slowly over several minutes when a rapid rate is maintained. This effect is attributed to fatigue, which develops and dissipates with a slow, symmetric time course. The dynamics of these properties can now be directly studied with selective stimulation protocols, and have many implications for the understanding of nodal behavior in the context of supraventricular tachyarrhythmias.

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BACKGROUND: Adenosine is well known to depress atrioventricular (AV) nodal conduction, but the potential interactions between adenosine and functional AV nodal properties have not been explored. The purpose of the present study was to determine (1) whether exogenous adenosine modifies the rate-dependent properties of the AV node, (2) to what extent such changes underlie the actions of adenosine in an in vitro model of AV reentrant tachycardia (AVRT), and (3) the potential role of endogenous adenosine in rate-induced AV nodal responses. METHODS AND RESULTS: The functional properties of AV nodal recovery (defining the conduction delay of a single premature activation), facilitation (effect of short cycles on subsequent nodal recovery), and fatigue (slowly developing AV nodal delay at a rapid rate) were studied selectively in isolated, superfused rabbit and guinea pig cardiac preparations. Exogenous adenosine increased AV nodal fatigue and attenuated facilitation, resulting in tachycardia-dependent increases in AH interval and AV nodal effective refractory period (AVERP). In experimental AVRT, adenosine caused greater increases in tachycardia cycle length (T) and AVERP as tachycardia rate increased. AVRT was sustained when AVERP/T was < 1, and adenosine suppressed AVRT by increasing the slope of the AVERP/T versus tachycardia rate relation, causing the critical ratio of 1 to be attained at slower rates. A mathematical model incorporating quantitative descriptors of recovery, facilitation, and fatigue accounted for changes in AH interval, AVERP, tachycardia cycle length, and AVERP/T under control conditions and in the presence of adenosine. In the absence of exogenous adenosine, 8-phenyltheophylline (10 mumol/L), an adenosine receptor antagonist, did not alter recovery or facilitation but significantly reduced rate-related fatigue (by 31 +/- 8%, mean +/- SEM, P < .05, in rabbit hearts; 46 +/- 5%, P < .01, in guinea pig hearts). Combined inhibition of adenosine deaminase (with erythro-9-[2-hydroxy-3-nonyl]-adenine hydrochloride, 5 mumol/L) and adenosine uptake (with dipyridamole, 1 mumol/L) increased fatigue in the absence of exogenous adenosine by 57 +/- 20% (P < .05). CONCLUSIONS: We conclude that (1) exogenously administered adenosine increases AV nodal fatigue and reduces facilitation, without altering AV nodal recovery; (2) these changes cause rate-dependent AV nodal depression, which plays a role in adenosine's actions on experimental AVRT; and (3) endogenous adenosine receptor activation plays a role in physiological AV nodal fatigue. Adenosine's ability to terminate reentrant supraventricular tachycardia may be due, at least in part, to its ability to enhance the physiological conduction slowing that results from sustained increases in AV nodal activation rate.

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