ライフサイエンスコーパス: refractory period

1 l as Poisson spike trains with long absolute refractory periods).

2 e controls without affecting the ventricular refractory period.

3 led Ca(2)(+) release units (CRUs) with fixed refractory period.

4 hances excitability by reducing the neuronal refractory period.

5 reshold excitatory inputs were followed by a refractory period.

6 4x threshold determined the shortest atrial refractory period.

7 h S1-S2 = 5 to 10 ms earlier than the atrial refractory period.

8 ing breaths or the duration of the resulting refractory period.

9 n by research on the so-called psychological refractory period.

10 ivity correlated in part with this transient refractory period.

11 stribution, cutaneous triggering and lack of refractory period.

12 s is true of tails both before and after the refractory period.

13 cne5(+/0) mice), and 10% shorter ventricular refractory period.

14 tion, an activity that correlates with their refractory period.

15 AF stability independent of baseline atrial refractory period.

16 urements or changes in ventricular effective refractory period.

17 response failure and recovery, followed by a refractory period.

18 isolated after the clusters had entered the refractory period.

19 le of Ca2+-activated K+ (BK) currents in the refractory period.

20 triggered pacing stimuli during the absolute refractory period.

21 transition that expresses a threshold and a refractory period.

22 mol/L had no significant effect on effective refractory period.

23 re-excite the heart after expiration of the refractory period.

24 Ca2+ elevation to the onset of the prolonged refractory period.

25 ility, and increases in both tau(SD) and the refractory period.

26 lantable defibrillator electrodes during the refractory period.

27 ntial generation, reducing duration, and the refractory period.

28 itical determinant of the time course of the refractory period.

29 ositive potentials, and prolong the relative refractory period.

30 same S2-induced graded response prolongs the refractory period.

31 n S2 at intervals shorter than the effective refractory period.

32 atrial action potential duration and atrial refractory period.

33 ponent of the total duration of the relative refractory period.

34 inner limit, however, was not its effective refractory period.

35 TEP and JI observed in the non-regenerative refractory period.

36 closure kinetics, which reduce the neuron's refractory period.

37 erative capacity than the first, revealing a refractory period.

38 rical burst, and reduced activity during the refractory period.

39 potential repolarization and shortening the refractory period.

40 periods of nonresponsiveness indicative of a refractory period.

41 without a driving input pulse and exhibits a refractory period.

42 fore, potentially, cellular excitability and refractory periods.

43 id channel openings and subsequent prolonged refractory periods.

44 urther reprocessed during subsequent spindle refractory periods.

45 ion, the cycle of block and unblock shortens refractory periods.

46 t transformations, for example thresholds or refractory periods.

47 tes and (2) decreasing absolute and relative refractory periods.

48 hetic stimulation did not change ventricular refractory periods.

49 characteristics, atrial activation times and refractory periods.

50 s, and atrial, AV, and ventricular effective refractory periods.

51 reductions in CD16 expression and activation refractory periods.

52 (IC; conduction velocity, 2.4 +/- 0.2 m/sec; refractory period, 0.6 +/- 0.1 msec) and were inhibited

53 Patients with DWR had a shorter effective refractory period (138.8+/-13.4 versus 163.8+/-12.2 ms,

54 -adaptive shortening of the atrial effective refractory periods (14+/-13 versus 12+/-14 ms; P=0.11).

55 ses in noninfarct zone ventricular effective refractory period, 3% to 5% increases in infarct zone ve

56 r assaying p(r), which utilizes the synaptic refractory period--a brief 5-6 ms period following relea

57 s; p = 0.05) and ventriculo-atrial effective refractory periods (AC(VI): 97 +/- 21 ms; control: 127 +

58 er argue that temporally-coordinated spindle refractory periods across local networks facilitate the

59 .1+/-1.0 Hz), suggesting a large gradient in refractory periods across the BZ.

60 al stimulation shortens the atrial effective refractory period (AERP) and maintains atrial fibrillati

61 In pace/controls, atrial effective refractory period (AERP) at a drive cycle length (DCL) o

62 y in the preclinical rabbit atrial effective refractory period (AERP) model.

63 (AF)-induced shortening of atrial effective refractory period (AERP), we examined the potential of K

64 te-dependent effects on the atrial effective refractory period (AERP).

65 Atrial effective refractory period, AF inducibility, and duration of indi

66 on to sinus rhythm included atrial effective refractory periods, AF cycle lengths, left atrial dimens

67 The duration of the refractory period affected only the low-frequency portio

68 ration and conduction time and the effective refractory period after delivery of the basic stimulus (

69 atrial premature beats and directly measured refractory periods after cardioversion) also increased f

70 table EBZ, pinacidil shortened the effective refractory period and abolished conduction block at shor

71 Effects on refractory period and AF duration in open chest pigs: Th

72 Atrial effective refractory period and AF inducibility on single extrasti

73 Effective refractory period and APD are closely related in the hum

74 three modified models that have no explicit refractory period and examine their ability to produce r

75 Nonactivity-dependent responses (refractory period and latency) at two stages of the circ

76 ntagonists and had a characteristic postwave refractory period and spatial boundaries between adjacen

77 The first peak indicates a refractory period and the 400 Hz oscillation demonstrate

78 s recovery function vanishes for an absolute refractory period and then gradually increases to unity.

79 of reentry necessitates a sufficiently short refractory period and/or delayed conduction, and AF has

80 of AP14145 and vernakalant on the effective refractory periods and acute burst pacing-induced AF wer

81 fast inactivated states, thereby shortening refractory periods and permitting rapid, repetitive, and

82 dren had similar accessory pathway effective refractory periods and supraventricular tachycardia indu

83 axons are adapted to produce extremely short refractory periods and that brief bursts of forward-prop

84 uences were used to measure atrioventricular refractory periods and to produce atrial echoes and epis

85 ction potential waveforms, automaticity, and refractory periods and, in most cardiac cells, multiple

86 reases in infarct zone ventricular effective refractory period, and 4% to 6% increases in QTc interva

87 ization, fast after-hyperpolarization, brief refractory period, and high firing frequency characteris

88 ngation of P-wave duration, increased atrial refractory period, and slowed atrial conduction.

89 rugs prolong the atrial action potential and refractory period, and thereby prevent recurrent atrial

90 The changes in AVNW-CL, AV nodal effective refractory period, and ventricular response during AF we

91 terval, from 2 to 45 ms beyond the effective refractory period, and was associated with unidirectiona

92 o investigate conduction patterns, effective refractory periods, and inducibility of AF.

93 overy of AP excitability during the relative refractory period; and steady-state INa inactivation via

94 site and the other MAPs, and PRR (effective refractory period-APD90=PRR) and related to the inductio

95 tently (receptive period approximately 1 wk; refractory period approximately 3 wk).

96 ivity-dependent depression and we identify a refractory period ( approximately 2 s) after endogenous

97 fective refractory period (ERP) and absolute refractory period (ARP) were significantly longer in dog

98 The effective and absolute refractory periods (ARP and ERP) were measured during an

99 produced AP shortening and reduced effective refractory period associated with altered IKs kinetics i

100 nized atrial electrograms and long effective refractory periods associated with disorganized electrog

101 tive refractory period, with short effective refractory periods associated with organized atrial elec

102 The effective refractory period at the high right atrium remained unch

103 ect not related to a change in the effective refractory period at the site of block.

104 us 376 +/- 466 ms; P=0.86), atrial effective refractory periods at 90 bpm (250+/-32 versus 248+/-36 m

105 vention was prolongation of atrial effective refractory periods, at least in part attributable to the

106 The majority (95% SUNCT and 89% SUNA) had no refractory period between attacks.

107 The difference in the effective refractory period between the high right atrium and the

108 changes in heart rates and atrial effective refractory period, but both significantly increased AF s

109 We demonstrate that the duration of the refractory period-but neither the cycle period nor the m

110 ociated with a prolongation of the effective refractory period by 18 +/- 2 ms (P < .05), an increase

111 Cooling increased the relative refractory period by 7.8% per degree C (P < 0.0001), slo

112 rrent treatments extend the atrial effective refractory period by nonselective blockade of cardiac io

113 d APD(-61 mV) (reflecting cellular effective refractory period) by 22% (P < 0.05 for each).

114 The refractory period can be manipulated, for example from 1

115 areas of the EBZ, nor was the EBZ effective refractory period changed.

116 rated significant prolongation of the atrial refractory period compared with vehicle controls without

117 d ventricular (117 versus 77.5 ms) effective refractory periods, compared with controls.

118 wave fronts, we found that the cycle length, refractory period, conduction velocity, and wavelength a

119 for 45 minutes to determine atrial effective refractory periods, conduction velocity, conduction hete

120 as the spontaneous activation rate and sAHP refractory period contribute to critical wave size varia

121 ms (type I) and the longest atrial effective refractory period corresponding to disorganized atrial e

122 y period, with the shortest atrial effective refractory period corresponding to organized atrial elec

123 The effective refractory period data were used to determine the inters

124 Concurrently, the right effective refractory period decreased.

125 nged action potential duration and effective refractory period, decreased LSG function were identifie

126 The effective refractory period difference between the sites of pacing

127 the site with the shortest atrial effective refractory period, disorganized atrial electrograms were

128 Increasing refractory period dispersion without changing conduction

129 ton arrival and emergence of a QB), and (iv) refractory period distribution (time for a microvillus t

130 in male SP expression levels correlate with refractory period duration in females, it is unknown whe

131 n on ventricular myocardial action potential refractory period, duration, force and rhythm is evidenc

132 re: starting and minimum pressure, burst and refractory period durations, enhanced contractile activi

133 gest decreased excitability and an increased refractory period during HF.

134 nconsistent with accounts of a psychological refractory period during sequential information processi

135 e to blood-borne bacteria was induction of a refractory period during which leukocyte activation by s

136 followed by a prolonged (approximately 18 h) refractory period during which the ability of both elect

137 ed pacing was again instituted, below atrial refractory period, during 2 min of apnea.

138 itation evoked is followed by a long-lasting refractory period, during which the previously excited n

139 ) activation of a signaling component with a refractory period (e.g. G protein), and 3) inactivation

140 he antegrade atrioventricular node effective refractory period (ERP) (from 252+/-60 to 303+/-70 ms; P

141 eity (p < 0.001); no change in the effective refractory period (ERP) (p > 0.8) or ERP heterogeneity (

142 lar (RV) and left ventricular (LV) effective refractory period (ERP) and absolute refractory period (

143 , and their effects on ventricular effective refractory period (ERP) and arrhythmia development were

144 uration (APD90), right ventricular effective refractory period (ERP) and blood pressure measurements

145 rillation (AF) shortens the atrial effective refractory period (ERP) and predisposes to further episo

146 Standard restitution, effective refractory period (ERP) and VF threshold (VFT) were meas

147 vide a surrogate for measuring the effective refractory period (ERP) in human ventricle.

148 de of membrane currents on APD and effective refractory period (ERP) in rat endocardial and epicardia

149 length, obese patients had shorter effective refractory period (ERP) in the left atrium (251 +/- 25 m

150 e action potential duration and/or effective refractory period (ERP) is thought to decrease the cycle

151 Because the effective refractory period (ERP) of the working myocardium is dif

152 le, AP duration (APD) restitution, effective refractory period (ERP) restitution, and conduction velo

153 The effect of effective refractory period (ERP) shortening on the vulnerability

154 repeat attempts at inducing AF and effective refractory period (ERP) testing.

155 ction potential duration (APD) and effective refractory period (ERP) than a noninducing site, resulti

156 LAA effective refractory period (ERP) was measured before and after pa

157 ng AF and the width, area, weight, effective refractory period (ERP), and wavelength in atrial tissue

158 Atrial effective refractory period (ERP), conduction velocity, wavelength

159 tential durations (APD(50,75,90)), effective refractory period (ERP), post repolarization refractorin

160 While approaching the effective refractory period (ERP), the tissue response is characte

161 n (APD), conduction velocity (CV), effective refractory period (ERP), tissue excitation threshold and

162 ted with attenuation of the atrial effective refractory period (ERP).

163 tructed restitution curves for the effective refractory period (ERP).

164 trial and ventricular effective and relative refractory periods (ERPs and RRPs) were significantly sh

165 ls (APs) at 90% repolarization and effective refractory periods (ERPs) (60 +/- 1 ms vs. 44 +/- 1 ms;

166 Effective refractory periods (ERPs) were determined at 5 myocardia

167 The effective refractory periods (ERPs) were measured in the setting o

168 ropranolol (0.1 mg/kg), and atrial effective refractory periods (ERPs) were obtained at baseline (EPS

169 Measurements of refractory period extension by shocks during ventricular

170 These findings support the refractory period extension hypothesis for defibrillatio

171 A relative refractory period followed CICR.

172 n produced by each impulse, but with a short refractory period following each Triggered impulse.

173 the AF vulnerability zone and the effective refractory period for a BCL, decreased as BCL lengthened

174 F every 6 h, which falls within the putative refractory period for biochemical responses, resulted in

175 RATIONALE: The development of a refractory period for Ca(2+) spark initiation after Ca(2

176 A refractory period for Ca(2+) spark initiation and subseq

177 During the refractory period for Hsp70 induction, HSF (heat-shock t

178 munity observed at P45 is reminiscent of the refractory period for inhibitory plasticity reported by

179 plasticity, demonstrating the presence of a refractory period for the regulation of synaptic plastic

180 ery ligation in dogs, ventricular functional refractory periods (FRPs) were measured at five to eight

181 e first evoked burst, with no evidence for a refractory period greater than approximately 1 s, even w

182 n potentials, resulting in shorter effective refractory periods, greater beat-to-beat variability of

183 n potentials, resulting in shorter effective refractory periods, greater beat-to-beat variability of

184 o the failing myocardium during the absolute refractory period improved LV function without increasin

185 , endocardial APD90 or ventricular effective refractory period in Scn5a+/Delta and WT hearts followin

186 t first transcriptional burst, followed by a refractory period in the range of hours.

187 ion-potential duration (APD) and abbreviated refractory period in the SQTS-hiPSC-CMs.

188 VIP shortens atrial effective refractory periods in dogs.

189 hearts, and prolonged ventricular effective refractory periods in initially non-arrhythmogenic Scn5a

190 he first-degree AV block dose, AVN effective refractory period increased from 186+/-37 to 282+/-33 ms

191 ssure during apnea were abolished, effective refractory period increased to 126.7+/-26.9 ms ( P=0.000

192 Effective refractory periods increased from 149+/-16 to 208+/-26 m

193 suring prolongation of ventricular effective refractory period induced by bilateral vagal stimulation

194 l DeltaPsim loss because of the disparity of refractory periods inside and outside the metabolic sink

195 whether the BK current is altered during the refractory period, intact clusters were stimulated to af

196 In excitable tissues the refractory period is a critical control mechanism preven

197 A shortened beta-cell replication refractory period is also observed.

198 o investigations have demonstrated that this refractory period is due in large part to the persistent

199 Effective refractory period is most closely reflected by APD70.

200 e SR, electrical inhibition is released, the refractory period is terminated and peristaltic contract

201 The inclusion of absolute refractory periods is not a satisfactory solution since

202 ven its association with a reduced effective refractory period, it may contribute to the substrate fo

203 Absolute and relative refractory periods largely accounted for the reliability

204 Furthermore, we identified a transient refractory period (lasting up to 120 min) following prec

205 The refractory period lasts only one to a few milliseconds,

206 LLDs are followed by a long refractory period, limiting LLD generation to approximat

207 In vivo, this refractory period limits the frequency of reproductive b

208 I ECG (hazard ratio [HR]: 4.20), ventricular refractory period <200 ms (HR: 3.91), and QRS fragmentat

209 G, history of syncope, ventricular effective refractory period <200 ms, and QRS fragmentation seem us

210 rial pacing</=250 ms (or antegrade effective refractory period</=250 ms if shortest preexcited RR int

211 e PEI comprises absolute and relative sexual refractory periods marked, respectively, by the presence

212 What happens during this "refractory period" might hold the key to spinal cord reg

213 uscles neither the mechanisms underlying the refractory period nor the link between excitability and

214 e that the global effect of VOR results in a refractory period of >/= 24 hours.

215 ne (< or =0.01 microL L(-1)) with a relative refractory period of 5 h after ethylene is added.

216 we investigated the relationship between the refractory period of a neuron and its firing precision.

217 ing of the action potential, the post-firing refractory period of a neuron and strength modulated fre

218 This previously unknown refractory period of ADCP, or hypophagia, was observed i

219 A postburst refractory period of circa 2 seconds that increases with

220 We observed a refractory period of neuronal origin in a two-stimuli pa

221 s (as was previously believed), produced the refractory period of spontaneous retinal waves and set t

222 identified an optimal anterograde effective refractory period of the accessory pathway cutoff of 240

223 +-sensitive K+ (BK) channels, determines the refractory period of the action potential.

224 Moreover, the refractory period of the afterdischarge itself may also

225 +/- 104 ms, P < .0001), as did the effective refractory period of the AV node (279 +/- 60 versus 304

226 hannel activity contributes to the prolonged refractory period of the bag cell neurons.

227 bility of food by significantly reducing the refractory period of the brain's feeding circuitry.

228 The relative and effective refractory period of the His-Purkinje system increased i

229 free firing rate derived by allowing for the refractory period often exceeded the observed firing rat

230 n used to predict the effect of removing the refractory period on a cell-by-cell basis for two largel

231 The refractory period opposes saturation, dynamically and st

232 synaptic factors are unlikely to explain the refractory period or its modulation by Ca(2+).

233 AF had shorter left atrial APD and effective refractory period (p = 0.01).

234 ted with a short accessory pathway antegrade refractory period (P<0.001) and atrioventricular reentra

235 rated that short accessory-pathway effective refractory period (P<0.001) and atrioventricular reentra

236 s showed shorter accessory-pathway effective refractory period (P<0.001) and more often exhibited mul

237 P<0.0003), and reduction in atrial effective refractory periods (P<0.0001) compared with control.

238 Furthermore, the duration of the refractory period predicts the timing of the next activa

239 After stimulation, T cells enter a transient refractory period, promoted by IL-2, during which they a

240 This refractory period provides a simple explanation for not

241 y, refractoriness, such as the Psychological Refractory Period (PRP) has only been quantified in disc

242 es (from depleted ROS) and induces (from the refractory period) regeneration, TEP increase and JI rev

243 It also shows that egg laying and refractory period response to SP is at least partially u

244 pression of RA by pacing during the absolute refractory period results in a significant reduction in

245 ntervals (AIs) in VF may depend on the local refractory period (RP), and sustained VF may require a s

246 ured at the pacing site and was shorter than refractory periods (RPs) near the base, creating heterog

247 From each VRC was measured the relative refractory period (RRP), the supernormality and the time

248 ulation was at the beginning of the relative refractory period (RRP), transitional make-break stimula

249 al upstroke, a prolongation of the effective refractory period secondary to the development of postre

250 The atrial effective refractory period shortened in ATR and CAF groups.

251 Atrial effective refractory period shortened progressively from 78+/-3 ms

252 Apnea-induced effective refractory period shortening from 110.20+/-31.3 ms to 90

253 er establishing chronic AF, atrial effective refractory period shortening, increases in spontaneous P

254 Using vagally induced atrial effective refractory period shortening, slowing of spontaneous sin

255 in the PCL shortened atrial and ventricular refractory periods significantly more than did the incre

256 nchronize (bursts) and generate a population refractory period (silence).

257 llatory stimulation, NFLs but not IFFLs show refractory-period stabilization (robustness to changes i

258 stimulations induce PIP3 responses without a refractory period, suggesting that GPCR-mediated inhibit

259 duced gene expression nor for the subsequent refractory period, suggesting that these phenomena depen

260 circuit, the resulting changes in effective refractory periods tend to stabilize reentry in this rem

261 ammed extra stimuli at 10 ms above effective refractory period than with stable pacing (13.4 +/- 16.5

262 ctive of the length of the stimulation and a refractory period that is shared with that generated by

263 niform self-renewal, slowed by a replication refractory period that prevents beta cells from immediat

264 ics was limited by absolute and relative tic refractory periods that were derived from an internal st

265 Given the tight distribution of refractory periods, the ability of refractoriness to imp

266 eled as probabilistic firing combined with a refractory period: the instantaneous firing rate is the

267 ulnerability zone for a BCL was its relative refractory period; the inner limit, however, was not its

268 ther rate-limiting step that may impact this refractory period, thereby providing an additional regul

269 tion bottleneck underlying the psychological refractory period to a frontoparietal network.

270 t effect on postsynaptic spiking, as did the refractory period to a smaller extent.

271 The ratio of the refractory period to the stimulus period predicted the i

272 We also measured ventricular effective refractory period (V-ERP) and QT interval in separate gr

273 lthough action potential shapes and relative refractory periods varied little between genotypes, Kv1.

274 lar fibrillation (VF), ventricular effective refractory period (VERP) and defibrillation threshold (D

275 a prolongation of the ventricular effective refractory period (VERP) in the models, although there m

276 hearts, and prolonged ventricular effective refractory periods (VERPs) in non-arrhythmogenic Scn5a+/

277 ammed extra stimuli at 10 ms above effective refractory period versus 66.1 +/- 22.9 ms with pacing at

278 Under these conditions, the refractory period was 147 ms; the action potential durat

279 l electrogram type with the atrial effective refractory period was further demonstrated by the effect

280 uced by more than fourfold, and the relative refractory period was increased in AdHERG-infected myocy

281 open-chest study, left-atrial (LA) effective refractory period was reduced similarly with AFL, AF+AFL

282 However, the refractory period was transient as a later fourth transf

283 el of cardiac action potential, in which the refractory period was variably shortened by a progressiv

284 ion, but not differences in atrial effective refractory periods, was associated with the development

285 dal function and right ventricular effective refractory period were impaired in the mutant mice, wher

286 DeltaV(m) produced by shocks in the absolute refractory period were measured with electrodes and a la

287 atrial fibrillation and the atrial effective refractory period were obtained from multiple sites of t

288 In the present study, auditory refractory periods were compared in a group of 24 young

289 setting response curves and atrial effective refractory periods were determined with single extrastim

290 In simulations, longer refractory periods were found to make the response more

291 Effective refractory periods were increased homogeneously througho

292 Refractory periods were tightly distributed, with a mean

293 ining disease dynamics is illustrated during refractory periods, when population susceptibility level

294 d at sites with the longest atrial effective refractory period, whereas 1:1 atrial capture was still

295 to contribute to pacemaker potentials and to refractory periods which control the rhythmical motility

296 roadening the action potential lengthens the refractory period, which may in turn be antiarrhythmogen

297 s) and extraordinarily long (more than 10 s) refractory periods, which prevent urine reflux and kidne

298 location are related to the atrial effective refractory period, with short effective refractory perio

299 losely followed that of the atrial effective refractory period, with the shortest atrial effective re

300 olonged atrial action potential duration and refractory period without affecting ventricular electrop