ライフサイエンスコーパス: action potential duration

1 ractoriness and spatiotemporal dispersion of action potential duration).

2 ial (RMP) without significant alterations in action potential duration.

3 sialylation leads to a 50-70-ms decrease in action potential duration.

4 f cultured human cardiomyocytes and shortens action potential duration.

5 atrial myocytes, with a parallel decrease in action potential duration.

6 d outward K(+), currents and a shortening of action potential duration.

7 or regulation of the cardiac IKs current and action potential duration.

8 n potential plateau potential, and prolonged action potential duration.

9 NH2-G628S eliminated AF by prolonging atrial action potential duration.

10 Y K 8644-induced prolongation of the cardiac action potential duration.

11 ype 2 syndrome by shortening the ventricular action potential duration.

12 assium current (I(Kur)) that controls atrial action potential duration.

13 crease in spontaneous rate and a decrease in action potential duration.

14 spersion of conduction velocity, but not the action potential duration.

15 and attenuates the regional heterogeneity of action potential duration.

16 ysis of an anti-Kv3.4 antibody prolonged the action potential duration.

17 tely 60%, a value similar to the decrease in action potential duration.

18 binding, Ca handling, L-type Ca current, and action potential duration.

19 enhanced cardiac excitability and prolonged action potential duration.

20 educed phase 0 upstroke slope, and prolonged action potential duration.

21 unction in the presynaptic space, modulating action potential duration.

22 s with a concomitant increase in ventricular action potential duration.

23 07-expressing adenovirus exhibited shortened action potential duration.

24 deactivation was not effective in modulating action potential durations.

25 slower action potential upstrokes and longer action potential durations.

26 ch compound caused shortening of ventricular action potential durations.

27 ormed to measure compound effects on cardiac action potential durations.

28 n of QT intervals and of ventricular myocyte action potential durations.

29 rom pyramidal neurons based on their briefer action potential durations.

30 CAND2 resulted in prolongation of the atrial action potential duration (17% and 45%, respectively).

31 lay a cycle length dependent prolongation of action potential duration (245 ms untreated, vs. 610 ms

32 g delayed repolarization and abnormally long action potential duration (312+/-30 ms versus 235+/-21 m

33 brafish resulted in shortening of the atrial action potential duration, a hallmark of AF.

34 Significant action potential duration abbreviation, secondary to fun

35 -term memory by calculating time constant of action potential duration accommodation (tau).

36 Increased dispersion of action potential duration across cardiac tissue has long

37 ugmentation of repolarizing I(NaK) dominates action potential duration adaptation and, in Pcell, I(Na

38 Thus, sex differences in K(+) channels and action potential durations alone cannot account for sex-

39 ery of CL(VF) was associated with discordant action potential duration alternans and induction of VF

40 Action potential duration alternans required progressive

41 Fast diffusion of V(m) keeps action potential duration alternans spatially synchroniz

42 tindole caused heterogeneous prolongation of action potential duration and a high incidence of early

43 from right ventricle demonstrated a shorter action potential duration and a lower Vmax in subepicard

44 in vitro show approximately 60% increase in action potential duration and a reduction in high-freque

45 These bursts vary in both frequency and action potential duration and also induce in situ ionic

46 lcium and peak sodium current, shortening of action potential duration and amplitude, increased cell

47 dium currents leading to prolongation of the action potential duration and an increased propensity to

48 pressing Nav1.5 p.H1849R displayed prolonged action potential duration and arrhythmogenic afterdepola

49 ed moderate atrial-selective prolongation of action potential duration and atrial-selective depressio

50 130G-CALM2, as shown by the normalization of action potential duration and Ca(2+)/CaM-dependent inact

51 new model replicates experimentally observed action potential duration and Ca(i) transient alternans

52 Restitution of action potential duration and conduction time and the ef

53 ial dispersion of refractoriness by reducing action potential duration and conduction time restitutio

54 rent I(Ca,L) steepened restitution curves of action potential duration and conduction velocity compar

55 utes; P<0.05), and incomplete restoration of action potential duration and conduction velocity early

56 Vm factors include electrical restitution of action potential duration and conduction velocity, short

57 he resting membrane potential with decreased action potential duration and contractility.

58 ons were associated with prolongation of the action potential duration and corrected QT interval.

59 nd becomes persistent, reflecting changes in action potential duration and densities of sodium, L-typ

60 Action potential duration and drug-induced arrhythmia we

61 with DMSO, concentration-dependent prolonged action potential duration and effective refractory perio

62 rkinje-like state characterized by prolonged action potential duration and expression of Purkinje-enr

63 ss requires large changes in the ventricular action potential duration and heart rate in mammals.

64 ibrillatory effect through shortening of the action potential duration and hyperpolarization of the c

65 versed the NE-stimulated decrease in cardiac action potential duration and increase in myocyte calciu

66 d both the NE-stimulated decrease in cardiac action potential duration and increase in myocyte calciu

67 ectrical remodeling contributes to prolonged action potential duration and increased incidence of arr

68 (and without) localized regions of decreased action potential duration and increased intercellular re

69 l mapping, whole-cell patch clamp to measure action potential duration and ionic currents, and quanti

70 toward the PV and stabilized at the shortest action potential duration and less-excitable region, con

71 very level of cardiovascular physiology from action potential duration and mitochondrial energetics t

72 ction mutations had heterogeneous effects on action potential duration and promoted early-after-depol

73 PD-118057 shortened the action potential duration and QT interval in arterially

74 ed to the discovery of agonists that shorten action potential duration and QT interval.

75 vented in miR-133a transgenic mice, although action potential duration and QT intervals did not refle

76 The presence of 3 muM PD-118057 prevented action potential duration and QT prolongation caused by

77 ty to known cardiotoxic drugs as measured by action potential duration and quantification of drug-ind

78 orylation), reducing EPSCs and so increasing action potential duration and reducing transmission fide

79 ium current causes heterogeneously prolonged action potential duration and rotors, as well as wave an

80 mal conditions and/or rapid pacing, both the action potential duration and the peak Ca concentration

81 dominance of the HERG channel in controlling action potential duration and the QT interval.

82 time, been able to accurately reproduce the action potential duration and the steady-state sodium co

83 K,ATP), consequently shortening the cellular action potential duration and ultimately suppressing ele

84 rvation and were optically mapped to measure action potential durations and DOR (apex-base) over the

85 ator causes dose-dependent shortening of the action potential durations and is able to normalize acti

86 in tissues with heterogeneously distributed action potential durations and then assessed the relativ

87 lular calcium and potassium ions, prolonging action-potential duration and increasing susceptibility

88 tly increased conduction velocity, shortened action potential duration, and [Ca(2+)]i transients dura

89 a(+) channels, where expression is linked to action potential duration, and associated with different

90 -type Ca current inactivation, did not alter action potential duration, and caused delayed afterdepol

91 perties (e.g., action potential propagation, action potential duration, and conduction velocity), dis

92 Vm mapping showed that conduction velocity, action potential duration, and dVm/dtmax were similar in

93 predict how changes in ionic currents alter action potential duration, and these were tested experim

94 ailability and therefore, cell excitability, action potential duration, and velocity of impulse propa

95 periods, greater beat-to-beat variability of action potential durations, and increased dispersion of

96 periods, greater beat-to-beat variability of action potential durations, and increased dispersion of

97 st plating to obtain conduction velocity and action potential duration (APD(70)).

98 ith the occurrence of spatially out-of-phase action potential duration (APD) alternans (discordant al

99 SR Ca(2+) and action potential duration (APD) alternans occurred in-ph

100 ) inactivation rate constant (kiCa) produced action potential duration (APD) alternans seen clinicall

101 d, and the propensity and characteristics of action potential duration (APD) alternans were investiga

102 ed in which regions with a large-small-large action potential duration (APD) alternate out-of-phase a

103 During spatially discordant alternans, the action potential duration (APD) alternates out of phase

104 that rate-dependent changes (restitution) in action potential duration (APD) and activation latency a

105 Our goal is to quantify LV/RV differences in action potential duration (APD) and APD rate adaptation

106 ions of I(Kr)-blocking drugs to increase the action potential duration (APD) and beat-to-beat variabi

107 on elicits a beat-to-beat alternation in the action potential duration (APD) and calcium (Ca) transie

108 lated from failing hearts is prolongation of action potential duration (APD) and conduction slowing.

109 ay and enhanced late INa (INa-L) prolong the action potential duration (APD) and contribute to early

110 Spatially discordant alternans, where the action potential duration (APD) and intracellular calciu

111 cally modified, and the resulting changes in action potential duration (APD) and its short term varia

112 apts to rate changes primarily by changes in action potential duration (APD) and morphology, while fo

113 action potential waveform-such as decreased action potential duration (APD) and plateau height-were

114 with high-performance liquid chromatography; action potential duration (APD) and rate dependent adapt

115 rmal TWA is linked with steep restitution of action potential duration (APD) and that both predict ar

116 ardial (EPI)-predominant prolongation of the action potential duration (APD) at 50% and 90% repolariz

117 By optical mapping techniques, action potential duration (APD) at 80% of repolarization

118 We determined transmural action potential duration (APD) before and after 100 nmo

119 Here, we report that CO prolongs action potential duration (APD) by inhibiting a subset o

120 atch-clamp studies show that prolongation of action potential duration (APD) can be further enhanced

121 the hypothesis that in normal hearts, local action potential duration (APD) determines local repolar

122 d condition characterized by prolongation of action potential duration (APD) in cardiac myocytes, pro

123 ed animals in vivo with corresponding longer action potential duration (APD) in cardiomyocytes incuba

124 he effect of mental challenge on ventricular action potential duration (APD) in conscious healthy hum

125 y can produce spatially dependent changes in action potential duration (APD) in homogeneous and isotr

126 ed major differences between groups, because action potential duration (APD) in T2DM failed to underg

127 tch clamp experiments showed prolongation of action potential duration (APD) in TAC and leptin-treate

128 We optically mapped the action potential duration (APD) in the coronary-perfused

129 ent blockade induces differential effects on action potential duration (APD) in the endocardium and e

130 Spatial dispersion of action potential duration (APD) is a substrate for the m

131 kinase (PI3K) signaling, which regulates the action potential duration (APD) of individual myocytes a

132 A beat-to-beat alternation in the action potential duration (APD) of myocytes, i.e. altern

133 ient at a given beat prolongs (shortens) the action potential duration (APD) of that beat.

134 We also observed substantial action potential duration (APD) prolongation and promine

135 l remodeling in heart failure is ventricular action potential duration (APD) prolongation.

136 fitted to action potential (AP) morphology, action potential duration (APD) restitution and conducti

137 ythmic effect by moderating the slope of the action potential duration (APD) restitution curve, by re

138 PACs may initiate AF if the rate response of action potential duration (APD) restitution has a slope

139 Construction of the action potential duration (APD) restitution portrait all

140 Action potential duration (APD) restitution properties a

141 nerve stimulation (VNS) reduces the slope of action potential duration (APD) restitution while simult

142 The upper and lower limits of vulnerability, action potential duration (APD) restitution, and conduct

143 nnels, plays an important role in post-shock action potential duration (APD) shortening and recurrent

144 hibitory peptide (AC3-I) unexpectedly showed action potential duration (APD) shortening.

145 At 90% repolarization, the action potential duration (APD) was 30.6 +/- 3.0 ms (n =

146 Action potential duration (APD) was significantly shorte

147 Acute and chronic dofetilide effects on action potential duration (APD) were studied in canine l

148 as beat-to-beat alternations in contraction, action potential duration (APD), and magnitude of the Ca

149 c nervous system (SNS) regulation of cardiac action potential duration (APD), mediated by beta-adrene

150 sed calcium influx in the mutation prolonged action potential duration (APD), produced steepened acti

151 kcne2 disruption prolonged ventricular action potential duration (APD), suggestive of reduced r

152 iodic beat-to-beat short-long alternation in action potential duration (APD), which is considered to

153 pstroke velocity and significantly prolonged action potential duration (APD).

154 makes it difficult to accurately measure the action potential duration (APD).

155 epolarization kinetics and prolonged cardiac action potential duration (APD).

156 d by tissue regions of high heterogeneity of action potential duration (APD).

157 the apex-to-base and transmural gradients of action potential duration (APD).

158 robust concentration-dependent reduction in action potential duration (APD).

159 ndromes that result from abnormal changes in action potential duration (APD).

160 Tertiapin prolonged action potential duration (APD; 54.7+/-24.0 to 128.8+/-1

161 Action potential durations (APD(50,75,90)), effective re

162 sion and hERG currents (IhERG) and shortened action-potential duration (APD).

163 rstood, but involve abnormal repolarization (action potential duration [APD]).

164 ed in cocultures compared with controls, but action potential duration (APD80) was not affected.

165 Ranolazine produced a prolongation of action potential duration (APD90) in atria, no effect on

166 Action potential durations (APDs) at 90% repolarization

167 Propagation latencies and action potential durations (APDs) from monophasic action

168 chnique was used to assess effects of VIP on action potential durations (APDs) in isolated canine lef

169 Optical mapping was used to measure action potential durations (APDs) in the presence of the

170 Moreover, conduction properties, action potential durations (APDs), and repolarizing curr

171 antial (>30 ms) shortening or lengthening of action potential duration as well as increased dispersio

172 The prominent AP prolongation at action potential duration at 30% repolarization level du

173 ts in the right atrium resulted in shortened action potential duration at 90% of repolarization (APD9

174 in LDLr(-/-) and ApoA1(-/-) than in WT mice (action potential duration at 90% of repolarization: 102+

175 , flattened CV restitution kinetics, reduced action potential duration at 90% recovery to baseline, i

176 type (WT), P < 0.001; n = 5) and endocardial action potential duration at 90% repolarication (APD90)

177 MI also produced a gradual reduction in action potential duration at 90% repolarization (APD(90)

178 In untreated Scn5a+/Delta hearts, epicardial action potential duration at 90% repolarization (APD90)

179 Monophasic action potential duration at 90% repolarization decrease

180 all electrical perturbations as evidenced by action potential duration at 90% repolarization variabil

181 ation, epileptic rats had longer ventricular action potential durations attributable to a sustained c

182 ich is presumably a consequence of shortened action potential duration because of reduced NCX activit

183 K(+) channel blockers increased reentry action potential duration but infrequently terminated re

184 on also affected transmural heterogeneity in action potential duration but not in [Ca(2+)]i transient

185 In atria, ranolazine slightly prolonged action potential duration but significantly depressed so

186 al support for compensatory normalization of action potential duration by a pharmacological agent.

187 rate that anti-Ro Abs inhibit IKr to prolong action potential duration by directly binding to the HER

188 lowed precisely controlled shortening of the action potential duration by switching on the light duri

189 depolarized resting V(m) and prolonged Na(+) action potential duration, by increasing its width and b

190 current (I(Ca,L)) is another determinant of action potential duration, Ca(2+) overload, early afterd

191 In addition, if action potential duration-Ca transients show quasiperiod

192 olated cardiomyocytes demonstrated prolonged action potential duration caused by reduced expression a

193 rmal repolarization of the wall, produced by action potential duration changes in the ischaemic regio

194 ayers showed altered conduction velocity and action potential duration compared with nontransduced an

195 myocytes, expression of S140G-IKs shortened action potential duration compared with WT-IKs.

196 c oscillations may cause oscillations in the action potential duration, creating the potential for ca

197 lcium channels and NMDA receptors to shorten action potential duration, dampen excitatory synaptic po

198 hyperkalemia, despite the shortening of the action potential duration, depolarization of E(K1) incre

199 tion resulting in the decrease of transmural action potential duration dispersion (64 +/- 12 ms versu

200 arrier and increased alternans magnitude and action potential duration dispersion, which may contribu

201 atients induced hyperpolarization, decreased action potential duration, enhanced early afterdepolariz

202 activity via deletion of BKbeta4 normalized action potential duration, excessive glutamate release a

203 icient to account for the large variation in action potential duration fluctuations observed in exper

204 We show that a critical gradient in action potential duration for conduction block can be an

205 Action potential duration for epicardial, mid-myocardial

206 Furthermore, dKO mice exhibited normalized action potential duration, glutamate release and short-t

207 ious electrophysiological parameters such as action potential duration gradients, refractoriness barr

208 uced a concentration-dependent shortening of action potential duration (>70%, 3 microM) that could be

209 We measured the action potential duration heterogeneity index and maxima

210 ential duration shortening and did not alter action potential duration in cells expressing WT-IKs.

211 arone and ranolazine caused little change in action potential duration in either chamber but induced

212 By shortening the action potential duration in HCM cardiomyocytes, ranolaz

213 tials in IB4 +ve, but dramatically increased action potential duration in IB4 ve, neurones.

214 rse SGK1's effects on NaV1.5 and shorten the action potential duration in induced pluripotent stem ce

215 ealed profound and selective prolongation of action potential duration in late-activated (288+/-29 ms

216 cially in lateral cells, and CRT abbreviated action potential duration in lateral but not anterior ce

217 from pancreatic beta-cells and in regulating action potential duration in muscle cells.

218 howed a reduced upstroke velocity and longer action potential duration in Scn5a-het myocytes.

219 Gain-of-function mutations shortened the action potential duration in single cells, and stabilise

220 utward conductance at the core and shortened action potential duration in the core vicinity, as well

221 Furthermore, Slob genotype influences action potential duration in vivo.

222 surface electrocardiographic recordings and action potential durations in isolated ventricular myocy

223 l/L) produced more significant shortening of action potential durations in RA (from 290+/-45 to 239+/

224 ctivation recovery interval (a surrogate for action potential duration) in the region close to the si

225 t variability of left-ventricular monophasic-action-potential duration increased after dofetilide (2.

226 s were perfused, mapped optically to analyze action potential durations, intracellular Ca(2)(+) trans

227 A beat-to-beat variation in the cardiac action potential duration is a phenomenon known as alter

228 -beat alternation (alternans) of the cardiac action potential duration is known to precipitate life-t

229 rdiomyocytes, which support the concept that action potential duration is uniform throughout the sarc

230 We find that the distribution of action potential durations is strongly bimodal.

231 e Na(+) current (INaL), although it prolongs action potential duration, is not by itself sufficient t

232 Based on action potential duration, juxtacellular labeling, and i

233 Action potential duration, L-type Ca2+ current, and Na+

234 ong that RNF207 is an important regulator of action potential duration, likely via effects on HERG tr

235 on-recovery intervals (a surrogate for local action potential duration; median, 275 versus 241 ms; P=

236 F1473S to mexiletine paradoxically increased action potential duration, mimicking QT prolongation see

237 radients in the currents resulted in shorter action potential duration, minimum diastolic potential t

238 s activity, and showed a gradual decrease in action potential duration (n=23).

239 plateau phase and is thus a key regulator of action potential duration of cardiomyocytes.

240 The composite action potential duration of heterogeneous tissue was we

241 d Kir2.1 expression, conduction velocity and action potential duration of the locally transduced and

242 f 2.5 Hz, and a variable prolongation of the action potential duration of up to several seconds.

243 both donor and failing hearts but shortened action potential duration only in failing hearts.

244 ored from glibenclamide-sensitive changes in action potential duration or intracellular free Mg2+.

245 Action potential duration oscillations originate primari

246 essor of miR-1 and Ito, leading to prolonged action potential duration post myocardial infarction.

247 en minimal reductions in function can extend action potential duration, prolong QT intervals, and ult

248 model, acute interstitial edema exacerbated action potential duration prolongation and produced EADs

249 gical conditions quantitatively predicts the action potential duration prolongation caused by exposur

250 Significant action potential duration prolongation was demonstrable

251 ing this fatal period manifested significant action potential duration prolongation, dispersion, and

252 n of RNF207 in zebrafish embryos resulted in action potential duration prolongation, occasionally a 2

253 epolarization dispersion caused by localized action potential duration prolongation.

254 despite similar left-ventricular monophasic-action-potential duration prolongations.

255 iques show a significant prolongation of the action potential duration prominently in late cardiac re

256 l approximated by an inverse sum of cellular action potential durations (R(2)=0.82).

257 ove 3 Hz, and cycle length dependence of the action potential duration, recapitulating key features o

258 ction potential and significantly reduce the action potential duration recorded in human cardiomyocyt

259 s reproducing changes in (dV(m)/dt)(max) and action potential duration required coupling to an HEK mo

260 Action potential duration restitution (APDR) and conduct

261 We hypothesize that apamin can flatten action potential duration restitution (APDR) curve and c

262 potential duration (APD), produced steepened action potential duration restitution (APDR) curves as w

263 In general, steep action potential duration restitution and broad conducti

264 t extrasystoles, particularly in relation to action potential duration restitution and conduction vel

265 te of highest dominant frequency had steeper action potential duration restitution and was more susce

266 ntly (p < 0.05) reduced the maximum slope of action potential duration restitution curve and converte

267 ates, and accurately reproduces experimental action potential duration restitution curves obtained by

268 eri-infarct zone exhibits regions with steep action potential duration restitution slope and unstable

269 Infusion of propranolol flattened action potential duration restitution, reduced wavebreak

270 hus helps to quantify the characteristics of action potential duration restitution.

271 ilure produced heterogeneous prolongation of action potential duration resulting in the decrease of t

272 g the effect of NE and ACh on rabbit cardiac action potential duration revealed that ACh blunted both

273 During coverslip ischemia, action potential duration shortened, Ca(i) transient dur

274 ponses to ischemia-reperfusion, with greater action potential duration shortening (P<0.001 at 8-minut

275 tion of HMR-1556 mitigated S140G-IKs-induced action potential duration shortening and did not alter a

276 nnel blocker, counteracted adenosine-induced action potential duration shortening and prevented AF in

277 and, in Pcell, I(NaL) contributes additional action potential duration shortening at short cycle leng

278 AF-induced I(Ca,L) downregulation and in the action potential duration shortening that maintains the

279 embrane potential within and near the PZ and action potential duration shortening throughout the vent

280 Measurements of action potential duration show a significantly decreased

281 sease, including prolongation of ventricular action potential duration, spontaneous early afterdepola

282 l mapping we observe increased dispersion of action potential duration, supersensitivity to beta-adre

283 reversed; however, females still have longer action potential durations than males.

284 s were assigned slower conduction and longer action potential durations than those for normal myocard

285 combine to synergistically increase cardiac action potential duration that is a likely cause of arrh

286 ons in Ca2+ cycling-inducing oscillations in action potential duration through Ca2+-sensitive conduct

287 citability, slowed conduction, and prolonged action potential duration until 90% repolarization (APD9

288 e organization and evolution of alternans in action potential duration using high-resolution optical

289 ial effects of leptin involve restoration of action potential duration via normalization of transient

290 First, calcium transient duration minus action potential duration was longer at subendocardium i

291 Action potential duration was prolonged in N-cad CKO ven

292 Action potential duration was shorter in hetKO with IKto

293 Conduction velocities were higher and action potential durations were significantly longer in

294 Action potential durations were significantly prolonged

295 Elimination of Kv4.3 also prolongs action potential duration, whereas the input resistances

296 ce between [Ca(2+)]i transients duration and action potential duration, which facilitates the formati

297 h muscle hyperpolarization and shortening of action-potential duration, which would limit calcium ent

298 l remodeling primarily through a decrease in action potential duration, while structural remodeling p

299 s associated with a dramatic prolongation of action potential duration with evidence of arrhythmic ac

300 Random cell-to-cell variations in action potential duration without EAD presence do not ca