ライフサイエンスコーパス: afterdepolarization

1 low-threshold burst firing driven by a spike afterdepolarization.

2 ane depolarization and the size of the spike afterdepolarization.

3 afterhyperpolarization and a longer-lasting afterdepolarization.

4 s the heart from arrhythmias due to sporadic afterdepolarizations.

5 t of APD and suppresses development of early afterdepolarizations.

6 isplayed prolonged repolarization with early afterdepolarizations.

7 rmalized the action potential, and prevented afterdepolarizations.

8 e by nonreentrant mechanisms such as delayed afterdepolarizations.

9 longation, increased I(Ca) facilitation, and afterdepolarizations.

10 ficant increase in the occurrence of delayed afterdepolarizations.

11 bility that resulted in formation of delayed afterdepolarizations.

12 tion and development of arrhythmogenic early afterdepolarizations.

13 tening, predisposing the myocardium to early afterdepolarizations.

14 f AP duration and provoked early and delayed afterdepolarizations.

15 hypokalemia, and quinidine resulted in early afterdepolarizations.

16 2 of the SCS occasionally resulted in early afterdepolarizations.

17 loss led to altered LTCC function and early afterdepolarizations.

18 low heart rate triggers arrhythmogenic early afterdepolarizations.

19 ses the myocardium to arrhythmogenic delayed afterdepolarizations.

20 ay be due to triggered activity from delayed afterdepolarizations.

21 longation and the induction of plateau early afterdepolarizations.

22 hich contributed to the development of early afterdepolarizations.

23 ) and generate triggered activity from early afterdepolarizations.

24 , which facilitates the formation of delayed afterdepolarizations.

25 ation of BFc inputs prolonged current-evoked afterdepolarizations.

26 carbon monoxide-induced proarrhythmic early afterdepolarizations.

27 action potential duration and arrhythmogenic afterdepolarizations.

28 (2+) exchanger activity and triggering early afterdepolarizations.

29 e similarly demonstrated increased INa-L and afterdepolarizations.

30 he action potential, and occurrence of early afterdepolarizations.

31 ility of repolarization and suppressed early afterdepolarizations.

32 eading to the formation of early and delayed afterdepolarizations.

33 on potentials, calcium transients, and early afterdepolarizations.

34 L, abbreviated the APD, and suppressed early afterdepolarizations.

35 ntial duration (APD) and contribute to early afterdepolarizations.

36 reduced the occurrence of early and delayed afterdepolarizations.

37 the APD and reducing the frequency of early afterdepolarizations.

38 ch as early afterdepolarizations and delayed afterdepolarizations.

39 Ca(2+) stores in the pathogenesis of delayed afterdepolarizations.

40 ased susceptibility to arrhythmia-triggering afterdepolarizations.

41 ting neurons was paralleled by a gradient in afterdepolarization (ADP) amplitude.

42 as a bifurcation parameter that reduces the afterdepolarization (ADP) and decreases the slope (gain)

43 ossy cells tested, and also produced a clear afterdepolarization (ADP) in nearly 100% of trials.

44 nderlying burst firing in these cells is the afterdepolarization (ADP) that follows each action poten

45 set of these interneurons was replaced by an afterdepolarization (ADP), often of sufficient magnitude

46 ramidal neurons are typically followed by an afterdepolarization (ADP), which in many cells contribut

47 proximal Na+ channels and a prominent spike afterdepolarization (ADP).

48 imulus train gave rise to an NMDAR-dependent afterdepolarization (ADP).

49 opamine D2 receptor (D2R) activation elicits afterdepolarizations (ADPs) in subcortically projecting

50 ring frequency and produced large, sustained afterdepolarizations (ADPs) of stratum oriens-lacunosum

51 tween the afterhyperpolarizations (AHPs) and afterdepolarizations (ADPs) that followed each action po

52 hat cause afterhyperpolarizations (AHPs) and afterdepolarizations (ADPs).

53 Intracellular recordings revealed a slow afterdepolarization (AfD) that triggers myotonic action

54 on to NMDA receptors, the quinpirole-induced afterdepolarization also depended on L-type Ca(2+) chann

55 olarizing potential (AHP) and increased slow afterdepolarization amplitudes (ADP), and reduced I(AHP)

56 ropagating action potential to attenuate the afterdepolarization and repetitive firing, axonal K(v)7

57 The spike-afterdepolarization and the generation of action potenti

58 xposure to the drug generated arrhythmogenic afterdepolarizations and >/=15-fold increases in INa-L.

59 We found that CsCl induced larger early afterdepolarizations and a greater prevalence of VT in d

60 Ca2+ overload occurring in ischemia leads to afterdepolarizations and aftercontractions that are resp

61 uM) increased the frequency and magnitude of afterdepolarizations and also led to development of trig

62 p the [Ca]SR below the threshold for delayed afterdepolarizations and arrhythmia.

63 sing Mg(2+) or flecainide eliminated delayed afterdepolarizations and decreased BVR independent of ef

64 on of drug-induced arrhythmias such as early afterdepolarizations and delayed afterdepolarizations.

65 respectively, compared with negligible early afterdepolarizations and ectopic beats in untreated cont

66 published studies using animal models, early afterdepolarizations and ectopic beats were observed in

67 inhibitor, did not reduce SCaEs and delayed afterdepolarizations and failed to prevent AF.

68 p to suppress arrhythmias initiated by early afterdepolarizations and premature beats in the ventricl

69 ced Na(+)/Ca(2+) exchanger-dependent delayed afterdepolarizations and spontaneous arrhythmias.

70 t genetic inhibition of NCX protects against afterdepolarizations and to investigate the underlying m

71 ly (1) reduced isoproterenol-induced delayed afterdepolarizations and triggered activity in infected

72 Early afterdepolarizations and triggered activity occurred spo

73 1), which predisposes HF myocytes to delayed afterdepolarizations and triggered activity.

74 marked arrhythmogenicity manifested by early afterdepolarizations and triggered arrhythmias, and redu

75 ction potential duration, and caused delayed afterdepolarizations and triggered beats in intact cardi

76 synaptic spikes are followed by a pronounced afterdepolarization, and are broadened by pharmacologica

77 ecrease the input resistance, shorten the AP afterdepolarization, and generate inhibitory postsynapti

78 de and faster AP rise rate, larger postspike afterdepolarization, and reduced membrane time constant.

79 action potential duration, spontaneous early afterdepolarizations, and 2:1 atrioventricular block in

80 ent (for a given SR Ca(2+) release), delayed afterdepolarizations, and nonreentrant initiation of ven

81 ith postpause action potential prolongation, afterdepolarizations, and triggered activity.

82 Afterdepolarizations apparently represent recurrent GABA

83 How delayed afterdepolarizations are synchronized to overcome the so

84 Delayed afterdepolarizations are thought to be due to spontaneou

85 Exposure to CO causes early afterdepolarization arrhythmias.

86 sed oxidative stress, CaMKII activation, and afterdepolarizations as triggers of lethal ventricular a

87 release have been shown to activate delayed afterdepolarizations as well as some cardiac arrhythmias

88 polarization response and augmentation of an afterdepolarization, both triggered by pirenzepine-sensi

89 Ca(2+) has been implicated in the genesis of afterdepolarizations, but pretreatment with high-dose W-

90 To confirm that D2Rs can elicit this afterdepolarization by enhancing Ca(2+) (and Ca(2+)-depe

91 This indicates that during delayed afterdepolarizations, Ca release units (CRUs) interact w

92 ntricle model, demonstrating that such early afterdepolarizations can propagate and initiate reentran

93 Early afterdepolarizations, considered cellular substrates for

94 Delayed afterdepolarizations could be induced easily and reversi

95 Phase 2 or 3 early afterdepolarizations could be induced easily by Bay K864

96 g early afterdepolarization (EAD) or delayed afterdepolarization (DAD) or both, is unknown.

97 s sarcoplasmic reticulum Ca release, delayed afterdepolarization (DAD), and triggered activity (TA) f

98 CR) from the sarcoplasmic reticulum, delayed-afterdepolarizations (DAD), and triggered activity.

99 arly afterdepolarizations (EADs) and delayed afterdepolarizations (DADs) are voltage oscillations kno

100 Delayed afterdepolarizations (DADs) carried by Na(+)-Ca(2+)-exch

101 holine (ACh) can elicit Ca2+-induced delayed afterdepolarizations (DADs) in atrial myocytes.

102 How early (EADs) and delayed afterdepolarizations (DADs) overcome electrotonic source

103 ) waves in cardiac myocytes underlie delayed afterdepolarizations (DADs) that trigger cardiac arrhyth

104 reticulum (SR) Ca(2+) release causes delayed afterdepolarizations (DADs) via Ca(2+)-induced transient

105 -sensitive inward currents to induce delayed afterdepolarizations (DADs).

106 ding to spontaneous Ca2+ release and delayed afterdepolarizations (DADs).

107 a(+)/Ca(2+)-exchanger activation and delayed afterdepolarizations (DADs).

108 In conclusion, H(2)O(2)-induced afterdepolarizations depend on both impaired I(Na) inact

109 ranolazine on late phase 3 early and delayed afterdepolarization (EAD and DAD)-induced triggered acti

110 his study examined the role of phase 2 early afterdepolarization (EAD) in producing a trigger to init

111 proarrhythmic effect, ie, by promoting early afterdepolarization (EAD) or delayed afterdepolarization

112 midal neurons in brain slices revealed early afterdepolarization (EAD)-like AP waveforms in CA1 but n

113 Exposure to H(2)O(2) initiated early afterdepolarization (EAD)-mediated triggered activity th

114 hearts showed that VT was initiated by early afterdepolarization (EAD)-mediated triggered activity.

115 Early afterdepolarizations (EADs) and delayed afterdepolarizat

116 lazine (5 to 20 micromol/L) suppressed early afterdepolarizations (EADs) and reduced the increase in

117 (3) Frequent epicardial early afterdepolarizations (EADs) and spontaneous ventricular

118 nous H(2)O(2) has been shown to induce early afterdepolarizations (EADs) and triggered activity by im

119 ated action potential can give rise to early afterdepolarizations (EADs) and triggered arrhythmia by

120 Spontaneous early afterdepolarizations (EADs) and ventricular tachycardia/

121 Pathologies that result in early afterdepolarizations (EADs) are a known trigger for tach

122 Early afterdepolarizations (EADs) are linked to both triggered

123 Cardiac action potential alternans and early afterdepolarizations (EADs) are linked to cardiac arrhyt

124 Early afterdepolarizations (EADs) are triggers of cardiac arrh

125 Early afterdepolarizations (EADs) are voltage oscillations tha

126 ecursor of lethal cardiac arrhythmias, early afterdepolarizations (EADs) during action potentials(APs

127 Irregularly occurring early afterdepolarizations (EADs) in cardiac myocytes are trad

128 Dofetilide (an IKr blocker) induced early afterdepolarizations (EADs) in female base myocytes cult

129 s to the development of arrhythmogenic early afterdepolarizations (EADs) in isolated cells and poorly

130 ation (APD) prolongation and prominent early afterdepolarizations (EADs) in neonatal cardiomyocytes e

131 tential prolongation, multiple foci of early afterdepolarizations (EADs) result in beat to beat chang

132 ted both to suppress and to facilitate early afterdepolarizations (EADs) when repolarization reserve

133 ce, and TG cardiomyocytes had frequent early afterdepolarizations (EADs), a hypothesized mechanism fo

134 membrane potential oscillations called early afterdepolarizations (EADs), and premature death in pace

135 n potential duration, Ca(2+) overload, early afterdepolarizations (EADs), and torsade de pointes.

136 Epicardial early afterdepolarizations (EADs), often accompanied by sponta

137 tracellular Ca2+ (Ca2+i) in triggering early afterdepolarizations (EADs), the origins of EADs and the

138 ormal electrical oscillations, such as early afterdepolarizations (EADs), which are associated with l

139 f the cardiac action potential causing early afterdepolarizations (EADs).

140 h in turn could promote delayed and/or early afterdepolarizations (EADs).

141 d beat-to-beat variability, leading to early afterdepolarizations (EADs).

142 tened susceptibility to arrhythmogenic early afterdepolarizations (EADs).

143 lihood of cellular arrhythmias such as early afterdepolarizations (EADs).

144 and late sodium current that produces early afterdepolarizations (EADs).

145 rolongation of APD and an incidence of early afterdepolarization equal to values previously reported

146 nd increases the propensity to develop early afterdepolarizations, especially in Endo.

147 cardiomyocyte action potentials and delayed afterdepolarizations, factors that increase risk of arrh

148 to trigger an action potential and the fast afterdepolarization following action potentials graduall

149 GABAergic and generate large I(CAN)-mediated afterdepolarizations following bursts of action potentia

150 Notably, we could still elicit this afterdepolarization for some time after the cessation of

151 ed action potential duration, enhanced early afterdepolarization formation, and facilitated triggered

152 ing [Na(+)]i monotonically increased delayed afterdepolarization frequency.

153 gene expression, and an increase in delayed afterdepolarizations from 0/min to 12/min.

154 hythmic substrate and triggers such as early afterdepolarization in experimental models.

155 The depolarization and slow afterdepolarization in GCs were blocked by the alpha1A-a

156 ings demonstrated the development of delayed afterdepolarizations in 69% of the CPVT-hiPSCs-CMs compa

157 The mechanisms leading to delayed afterdepolarizations in AF patients have not been define

158 ous Ca2+ release events that lead to delayed afterdepolarizations in affected patients.

159 frequency and amplitude of SCaEs and delayed afterdepolarizations in atrial myocytes and intact atria

160 f AF by promoting regional SCaEs and delayed afterdepolarizations in atrial tissue, which can be prev

161 dofetilide to increase APD and induce early afterdepolarizations in females.

162 , CORM-2-prolonged the APs and induced early afterdepolarizations in guinea pig myocytes.

163 ent is known to mediate arrhythmogenic early afterdepolarizations in heart, and these were similarly

164 entials and to a higher probability of early afterdepolarizations in MLP-/- than in control myocytes.

165 hypokalemia in the long term, or by delayed afterdepolarizations in the short term.

166 uM) and thapsigargin (10 muM) eliminated all afterdepolarizations in these cells.

167 ect to increase APD diminished, as did early afterdepolarization incidence.

168 or AP firing, increased incidence of delayed afterdepolarizations, increased calcium transient durati

169 nsistent with the greater incidence of early afterdepolarizations induced in this region by dofetilid

170 M cells and Purkinje fibers to develop early afterdepolarization-induced extrasystoles, which are tho

171 Our data suggest delayed afterdepolarization-induced extrasystolic activity serve

172 /RyR2(R4496C) mouse hearts generated delayed afterdepolarization-induced triggered activity at lower

173 se results support the hypothesis that early afterdepolarization-induced triggered activity in Purkin

174 esting that they might be initiated by early afterdepolarization-induced triggered activity in Purkin

175 This study sought to determine whether early afterdepolarization-induced triggered activity is respon

176 Delayed afterdepolarization-induced triggered beats that origina

177 Although it is widely accepted that afterdepolarizations initiate arrhythmias when action po

178 These ECG analyses suggest that early afterdepolarizations initiate TdP and, if present, may h

179 the inward aftercurrent underlying the slow afterdepolarization is inhibited by expression of a Galp

180 Surprisingly, this afterdepolarization is masked in quiescent brain slices,

181 We have shown previously that the muscarinic afterdepolarization is mediated by a calcium-activated n

182 ; (6) greater Pcell vulnerability to delayed afterdepolarizations is attributable to higher sarcoplas

183 ggered activity (apparently induced by early afterdepolarizations) is observed.

184 tation induced QT prolongation and transient afterdepolarizations, known cellular mechanisms for arrh

185 Mechanically induced delayed afterdepolarization-like events contributed to the forma

186 to PV BCs, CCK BCs exhibited a mAChR-induced afterdepolarization (mADP) that was frequency and activi

187 Moreover, the cholinergic engagement of afterdepolarizations may contribute to the formation of

188 at the onset of focal activity showed early afterdepolarization-mediated triggered activity that led

189 ontaneous VF arising from the RV by an early afterdepolarization-mediated triggered activity.

190 ly coupled action potentials consistent with afterdepolarization-mediated triggered beats were readil

191 rats and 2 of 9 normal rats (P<0.05); early afterdepolarization occurred in two CKD rats but not nor

192 hat were responsible for the prominent spike afterdepolarization of CA3 pyramids.

193 ntial duration and a high incidence of early afterdepolarizations on 1-Hz electric point stimulation,

194 ibers attributable to abnormal automaticity, afterdepolarizations, or reentry.

195 mulation induces a long-lasting subthreshold afterdepolarization, persistent firing, or prolonged pla

196 ncreased the amplitude of the postburst slow afterdepolarization potential (sADP) at the soma of both

197 It is clear that delayed afterdepolarization resulting from abnormal activation o

198 motoneurons displayed a characteristic slow afterdepolarization (sADP).

199 mediate the muscarinic receptor-induced slow afterdepolarization seen in pyramidal cells of the cereb

200 nce of beta stimulation, we observed delayed afterdepolarizations, suggesting that accelerated recove

201 bral cortex induces the appearance of a slow afterdepolarization that can sustain autonomous spiking

202 obust excitatory effect that included a slow afterdepolarization that followed a train of action pote

203 application of TRH prominently enhanced the afterdepolarization that follows rebound Ca2+ spikes, su

204 , the D2R agonist quinpirole elicits a novel afterdepolarization that generates voltage fluctuations

205 , D2Rs can elicit a Ca(2+)-channel-dependent afterdepolarization that powerfully modulates activity i

206 ction potential repolarization to produce an afterdepolarization that triggers subsequent action pote

207 4) have a propensity to develop phase 2 to 4 afterdepolarizations that can elicit triggered beats; an

208 The afterdepolarizations that initiate TdP are facilitated b

209 to contribute to the arrhythmogenic delayed afterdepolarizations that occur in Ca2+-overloaded cells

210 /Ca(2+) exchange current inducing a "delayed afterdepolarization" that can in turn trigger an action

211 s, in turn, is accompanied by arrhythmogenic afterdepolarizations thought to trigger torsades de poin

212 -clamp and Ca(2+) imaging, early and delayed afterdepolarizations trailed spontaneous Ca(2+) release

213 leading to increased vulnerability to early afterdepolarization, triggered activity, and ventricular

214 ing gain, causes AF-promoting atrial delayed afterdepolarizations/triggered activity in cAF patients.

215 panied by inward I(NCX) currents and delayed afterdepolarizations/triggered activity occurred more of

216 hat lead to focal ectopic firing via delayed afterdepolarizations/triggered activity.

217 -function increased [Ca2+]i and caused early afterdepolarizations under adrenergic stress, as observe

218 s underlying the muscarinic receptor-induced afterdepolarization using molecular biological and elect

219 the post-burst afterhyperpolarization to an afterdepolarization via a rapidly reversible upregulatio

220 The afterdepolarization was dependent on elevations in intra

221 -6) mol/L dofetilide, the incidence of early afterdepolarizations was 28% in DHT-treated and 55% in n

222 cle length=1 second), the incidence of early afterdepolarizations was: female, 67%; ORCH, 56%; male,

223 Early afterdepolarizations were more frequent in DHF than in c

224 Early afterdepolarizations were not accompanied by Ca(2+) wave

225 Early afterdepolarizations were observed after application of

226 ged significantly; and, in some cells, early afterdepolarizations were observed.

227 ction-potential (AP) durations after delayed afterdepolarizations were significantly prolonged.

228 s increased excitability and increased spike afterdepolarization, were affected by the training.

229 the RyR increased the probability of delayed afterdepolarizations when heart failure was simulated.

230 nd membrane potential, with signs of delayed afterdepolarizations when undergoing periodic pacing and

231 pontaneous Ca elevations (SCaEs) and delayed afterdepolarizations whenever the pacing train failed to

232 pression, where high [Na(+)]i causes delayed afterdepolarizations, which can be prevented by imposing

233 he elevated [Na(+)]i of PCs promoted delayed afterdepolarizations, which were always preceded by spon