戻る
「早戻しボタン」を押すと検索画面に戻ります。 [閉じる]

コーパス検索結果 (1語後でソート)

通し番号をクリックするとPubMedの該当ページを表示します
1 ractoriness and spatiotemporal dispersion of action potential duration).
2  enhanced cardiac excitability and prolonged action potential duration.
3  rectifier potassium currents and normalized action potential duration.
4 unction in the presynaptic space, modulating action potential duration.
5 s with a concomitant increase in ventricular action potential duration.
6 07-expressing adenovirus exhibited shortened action potential duration.
7 ial (RMP) without significant alterations in action potential duration.
8  in and a nonsignificant 15% prolongation of action potential duration.
9  sialylation leads to a 50-70-ms decrease in action potential duration.
10 f cultured human cardiomyocytes and shortens action potential duration.
11 atrial myocytes, with a parallel decrease in action potential duration.
12 d outward K(+), currents and a shortening of action potential duration.
13 or regulation of the cardiac IKs current and action potential duration.
14 n potential plateau potential, and prolonged action potential duration.
15 NH2-G628S eliminated AF by prolonging atrial action potential duration.
16 Y K 8644-induced prolongation of the cardiac action potential duration.
17 ype 2 syndrome by shortening the ventricular action potential duration.
18 assium current (I(Kur)) that controls atrial action potential duration.
19 crease in spontaneous rate and a decrease in action potential duration.
20 spersion of conduction velocity, but not the action potential duration.
21 and attenuates the regional heterogeneity of action potential duration.
22 tion of L-type Ca(2+) channels and prolonged action potential duration.
23 ERG potassium channel influences ventricular action potential duration.
24 ons and leads to substantial prolongation of action potential duration.
25 educed phase 0 upstroke slope, and prolonged action potential duration.
26 binding, Ca handling, L-type Ca current, and action potential duration.
27 deactivation was not effective in modulating action potential durations.
28 slower action potential upstrokes and longer action potential durations.
29 ch compound caused shortening of ventricular action potential durations.
30 ormed to measure compound effects on cardiac action potential durations.
31 n of QT intervals and of ventricular myocyte action potential durations.
32 CAND2 resulted in prolongation of the atrial action potential duration (17% and 45%, respectively).
33 lay a cycle length dependent prolongation of action potential duration (245 ms untreated, vs. 610 ms
34 g delayed repolarization and abnormally long action potential duration (312+/-30 ms versus 235+/-21 m
35 brafish resulted in shortening of the atrial action potential duration, a hallmark of AF.
36                                  Significant action potential duration abbreviation, secondary to fun
37 -term memory by calculating time constant of action potential duration accommodation (tau).
38                      Increased dispersion of action potential duration across cardiac tissue has long
39 enzalutamide (25 uM) significantly prolonged action potential durations (action potential duration at
40 ugmentation of repolarizing I(NaK) dominates action potential duration adaptation and, in Pcell, I(Na
41   Thus, sex differences in K(+) channels and action potential durations alone cannot account for sex-
42 ery of CL(VF) was associated with discordant action potential duration alternans and induction of VF
43                                              Action potential duration alternans required progressive
44 tindole caused heterogeneous prolongation of action potential duration and a high incidence of early
45  from right ventricle demonstrated a shorter action potential duration and a lower Vmax in subepicard
46  in vitro show approximately 60% increase in action potential duration and a reduction in high-freque
47      These bursts vary in both frequency and action potential duration and also induce in situ ionic
48 lcium and peak sodium current, shortening of action potential duration and amplitude, increased cell
49 dium currents leading to prolongation of the action potential duration and an increased propensity to
50 pressing Nav1.5 p.H1849R displayed prolonged action potential duration and arrhythmogenic afterdepola
51 ed moderate atrial-selective prolongation of action potential duration and atrial-selective depressio
52 130G-CALM2, as shown by the normalization of action potential duration and Ca(2+)/CaM-dependent inact
53 pecific characteristics, including increased action potential duration and cellular automaticity.
54 ial dispersion of refractoriness by reducing action potential duration and conduction time restitutio
55 utes; P<0.05), and incomplete restoration of action potential duration and conduction velocity early
56 he resting membrane potential with decreased action potential duration and contractility.
57 ons were associated with prolongation of the action potential duration and corrected QT interval.
58 ITAF overexpression simultaneously shortened action potential duration and decreased calcium transien
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 gent currents in DRG neurons greatly prolong action potential duration and enhance repetitive firing.
63 rkinje-like state characterized by prolonged action potential duration and expression of Purkinje-enr
64 ss requires large changes in the ventricular action potential duration and heart rate in mammals.
65 ibrillatory effect through shortening of the action potential duration and hyperpolarization of the c
66 d both the NE-stimulated decrease in cardiac action potential duration and increase in myocyte calciu
67 versed the NE-stimulated decrease in cardiac action potential duration and increase in myocyte calciu
68 ectrical remodeling contributes to prolonged action potential duration and increased incidence of arr
69 (and without) localized regions of decreased action potential duration and increased intercellular re
70  inward current, increases rheobase, extends action potential duration and increases synaptic inputs.
71 l amygdala (CeL), and its activity modulates action potential duration and inhibitory postsynaptic cu
72 l mapping, whole-cell patch clamp to measure action potential duration and ionic currents, and quanti
73 toward the PV and stabilized at the shortest action potential duration and less-excitable region, con
74 very level of cardiovascular physiology from action potential duration and mitochondrial energetics t
75 ction mutations had heterogeneous effects on action potential duration and promoted early-after-depol
76 ed to the discovery of agonists that shorten action potential duration and QT interval.
77 vented in miR-133a transgenic mice, although action potential duration and QT intervals did not refle
78 ty to known cardiotoxic drugs as measured by action potential duration and quantification of drug-ind
79                             Ang II prolonged action potential duration and reduced action potential u
80 orylation), reducing EPSCs and so increasing action potential duration and reducing transmission fide
81 ium current causes heterogeneously prolonged action potential duration and rotors, as well as wave an
82 ulum Ca(2+) stores attributable to a reduced action potential duration and sarcoendoplasmic reticulum
83 dominance of the HERG channel in controlling action potential duration and the QT interval.
84  time, been able to accurately reproduce the action potential duration and the steady-state sodium co
85 K,ATP), consequently shortening the cellular action potential duration and ultimately suppressing ele
86 ator causes dose-dependent shortening of the action potential durations and is able to normalize acti
87  in tissues with heterogeneously distributed action potential durations and then assessed the relativ
88 lular calcium and potassium ions, prolonging action-potential duration and increasing susceptibility
89 tly increased conduction velocity, shortened action potential duration, and [Ca(2+)]i transients dura
90 a(+) channels, where expression is linked to action potential duration, and associated with different
91 -type Ca current inactivation, did not alter action potential duration, and caused delayed afterdepol
92 perties (e.g., action potential propagation, action potential duration, and conduction velocity), dis
93  Vm mapping showed that conduction velocity, action potential duration, and dVm/dtmax were similar in
94  atrial arrhythmia susceptibility, prolonged action potential duration, and ectopic cardiomyocyte dep
95 pid delayed rectifier current I(Kr), prolong action potential duration, and induce potentially lethal
96  AF burden, restored I(Na), I(Ca,L), I(Kur), action potential duration, and reversed atrial fibrosis
97  predict how changes in ionic currents alter action potential duration, and these were tested experim
98 ailability and therefore, cell excitability, action potential duration, and velocity of impulse propa
99 periods, greater beat-to-beat variability of action potential durations, and increased dispersion of
100 periods, greater beat-to-beat variability of action potential durations, and increased dispersion of
101 st plating to obtain conduction velocity and action potential duration (APD(70)).
102 ed hearts, there were no differences in mean action potential duration (APD(80)) between groups; howe
103 ith the occurrence of spatially out-of-phase action potential duration (APD) alternans (discordant al
104                                SR Ca(2+) and action potential duration (APD) alternans occurred in-ph
105 ) inactivation rate constant (kiCa) produced action potential duration (APD) alternans seen clinicall
106 d, and the propensity and characteristics of action potential duration (APD) alternans were investiga
107 that rate-dependent changes (restitution) in action potential duration (APD) and activation latency a
108 Our goal is to quantify LV/RV differences in action potential duration (APD) and APD rate adaptation
109 ions of I(Kr)-blocking drugs to increase the action potential duration (APD) and beat-to-beat variabi
110                Adult hearts had the shortest action potential duration (APD) and Ca(2+) transient dur
111 on elicits a beat-to-beat alternation in the action potential duration (APD) and calcium (Ca) transie
112  current as a potential mechanism to prolong action potential duration (APD) and cause LQT9.
113 lated from failing hearts is prolongation of action potential duration (APD) and conduction slowing.
114 ay and enhanced late INa (INa-L) prolong the action potential duration (APD) and contribute to early
115 cally modified, and the resulting changes in action potential duration (APD) and its short term varia
116 apts to rate changes primarily by changes in action potential duration (APD) and morphology, while fo
117  action potential waveform-such as decreased action potential duration (APD) and plateau height-were
118 with high-performance liquid chromatography; action potential duration (APD) and rate dependent adapt
119 enerating a late Na(+) current that prolongs action potential duration (APD) and triggering proarrhyt
120 ardial (EPI)-predominant prolongation of the action potential duration (APD) at 50% and 90% repolariz
121               By optical mapping techniques, action potential duration (APD) at 80% of repolarization
122 ucting a probability density function of the action potential duration (APD) at different cycle lengt
123                     We determined transmural action potential duration (APD) before and after 100 nmo
124             Here, we report that CO prolongs action potential duration (APD) by inhibiting a subset o
125 atch-clamp studies show that prolongation of action potential duration (APD) can be further enhanced
126 ed animals in vivo with corresponding longer action potential duration (APD) in cardiomyocytes incuba
127 he effect of mental challenge on ventricular action potential duration (APD) in conscious healthy hum
128 y can produce spatially dependent changes in action potential duration (APD) in homogeneous and isotr
129 ed major differences between groups, because action potential duration (APD) in T2DM failed to underg
130 tch clamp experiments showed prolongation of action potential duration (APD) in TAC and leptin-treate
131                      We optically mapped the action potential duration (APD) in the coronary-perfused
132 ent blockade induces differential effects on action potential duration (APD) in the endocardium and e
133                        Spatial dispersion of action potential duration (APD) is a substrate for the m
134 kinase (PI3K) signaling, which regulates the action potential duration (APD) of individual myocytes a
135            A beat-to-beat alternation in the action potential duration (APD) of myocytes, i.e. altern
136 ient at a given beat prolongs (shortens) the action potential duration (APD) of that beat.
137                 We also observed substantial action potential duration (APD) prolongation and promine
138 l remodeling in heart failure is ventricular action potential duration (APD) prolongation.
139  fitted to action potential (AP) morphology, action potential duration (APD) restitution and conducti
140 ythmic effect by moderating the slope of the action potential duration (APD) restitution curve, by re
141 PACs may initiate AF if the rate response of action potential duration (APD) restitution has a slope
142 nnels, plays an important role in post-shock action potential duration (APD) shortening and recurrent
143      Acute and chronic dofetilide effects on action potential duration (APD) were studied in canine l
144 th electrophysiological changes that prolong action potential duration (APD) within the border zone (
145 as beat-to-beat alternations in contraction, action potential duration (APD), and magnitude of the Ca
146 sed calcium influx in the mutation prolonged action potential duration (APD), produced steepened acti
147       kcne2 disruption prolonged ventricular action potential duration (APD), suggestive of reduced r
148 iodic beat-to-beat short-long alternation in action potential duration (APD), which is considered to
149  robust concentration-dependent reduction in action potential duration (APD).
150 nel is a critical regulator of cardiomyocyte action potential duration (APD).
151 ndromes that result from abnormal changes in action potential duration (APD).
152 pstroke velocity and significantly prolonged action potential duration (APD).
153 channel (Cav1.2) is essential for cardiocyte action potential duration (APD).
154 d by tissue regions of high heterogeneity of action potential duration (APD).
155 the apex-to-base and transmural gradients of action potential duration (APD).
156 es exhibited average CVs of 14 +/- 0.6 cm/s, Action Potential Duration (APD)80 and APD30 of 152 +/- 1
157                          Tertiapin prolonged action potential duration (APD; 54.7+/-24.0 to 128.8+/-1
158                                              Action potential durations (APD(50,75,90)), effective re
159 racellular recordings demonstrated shortened action-potential duration (APD) and abbreviated refracto
160 sion and hERG currents (IhERG) and shortened action-potential duration (APD).
161 rstood, but involve abnormal repolarization (action potential duration [APD]).
162                                              Action potential durations (APDs) at 90% repolarization
163                    Propagation latencies and action potential durations (APDs) from monophasic action
164 chnique was used to assess effects of VIP on action potential durations (APDs) in isolated canine lef
165          Optical mapping was used to measure action potential durations (APDs) in the presence of the
166 antial (>30 ms) shortening or lengthening of action potential duration as well as increased dispersio
167             The prominent AP prolongation at action potential duration at 30% repolarization level du
168 ts in the right atrium resulted in shortened action potential duration at 90% of repolarization (APD9
169 in LDLr(-/-) and ApoA1(-/-) than in WT mice (action potential duration at 90% of repolarization: 102+
170 , flattened CV restitution kinetics, reduced action potential duration at 90% recovery to baseline, i
171 Q(+/-) myocytes (n=5) demonstrated prolonged action potential duration at 90% repolarization and afte
172 all electrical perturbations as evidenced by action potential duration at 90% repolarization variabil
173 cantly prolonged action potential durations (action potential duration at 90% when paced at 0.5 Hz; 4
174           Optical mapping revealed prolonged action potential duration at slower pacing cycle lengths
175 ation, epileptic rats had longer ventricular action potential durations attributable to a sustained c
176                                   Rise time, action potential duration, beat period, and triangulatio
177 ich is presumably a consequence of shortened action potential duration because of reduced NCX activit
178      K(+) channel blockers increased reentry action potential duration but infrequently terminated re
179 on also affected transmural heterogeneity in action potential duration but not in [Ca(2+)]i transient
180 ta or IL-6 in the absence of hMSCs prolonged action potential duration but only IL-6 increased Ca2+ a
181      In atria, ranolazine slightly prolonged action potential duration but significantly depressed so
182 th nonfailing hMSCs, failing hMSCs prolonged action potential duration by 24% (P<0.001, n=15), increa
183 al support for compensatory normalization of action potential duration by a pharmacological agent.
184 chronic inactivity homeostatically increases action potential duration by changing alternative splici
185 rate that anti-Ro Abs inhibit IKr to prolong action potential duration by directly binding to the HER
186 lowed precisely controlled shortening of the action potential duration by switching on the light duri
187                              In addition, if action potential duration-Ca transients show quasiperiod
188                Using fluorescent indicators, action potential duration, Ca2+ alternans, and spontaneo
189 olated cardiomyocytes demonstrated prolonged action potential duration caused by reduced expression a
190 ayers showed altered conduction velocity and action potential duration compared with nontransduced an
191 oplasmic reticulum Ca(2+) content, and short action potential duration compared with right ventricula
192  myocytes, expression of S140G-IKs shortened action potential duration compared with WT-IKs.
193 lcium channels and NMDA receptors to shorten action potential duration, dampen excitatory synaptic po
194  hyperkalemia, despite the shortening of the action potential duration, depolarization of E(K1) incre
195 tion resulting in the decrease of transmural action potential duration dispersion (64 +/- 12 ms versu
196 atients induced hyperpolarization, decreased action potential duration, enhanced early afterdepolariz
197  activity via deletion of BKbeta4 normalized action potential duration, excessive glutamate release a
198 icient to account for the large variation in action potential duration fluctuations observed in exper
199                                              Action potential duration for epicardial, mid-myocardial
200   Furthermore, dKO mice exhibited normalized action potential duration, glutamate release and short-t
201 uced a concentration-dependent shortening of action potential duration (&gt;70%, 3 microM) that could be
202                              We measured the action potential duration heterogeneity index and maxima
203  and ion current levels leading to shortened action potential duration in atrial cardiomyocytes compa
204  increase in outward K(+) currents decreased action potential duration in cardiomyocytes lacking PC1.
205                         PC1 ablation reduced action potential duration in cardiomyocytes, decreased C
206 ential duration shortening and did not alter action potential duration in cells expressing WT-IKs.
207 arone and ranolazine caused little change in action potential duration in either chamber but induced
208                            By shortening the action potential duration in HCM cardiomyocytes, ranolaz
209 tials in IB4 +ve, but dramatically increased action potential duration in IB4 ve, neurones.
210 rse SGK1's effects on NaV1.5 and shorten the action potential duration in induced pluripotent stem ce
211 cially in lateral cells, and CRT abbreviated action potential duration in lateral but not anterior ce
212 from pancreatic beta-cells and in regulating action potential duration in muscle cells.
213 howed a reduced upstroke velocity and longer action potential duration in Scn5a-het myocytes.
214     Gain-of-function mutations shortened the action potential duration in single cells, and stabilise
215        Furthermore, Slob genotype influences action potential duration in vivo.
216 ction of TASK-1 currents and prolongation of action potential durations in atrial cardiomyocytes to s
217  surface electrocardiographic recordings and action potential durations in isolated ventricular myocy
218 l/L) produced more significant shortening of action potential durations in RA (from 290+/-45 to 239+/
219 ctivation recovery interval (a surrogate for action potential duration) in the region close to the si
220 t variability of left-ventricular monophasic-action-potential duration increased after dofetilide (2.
221 s were perfused, mapped optically to analyze action potential durations, intracellular Ca(2)(+) trans
222      A beat-to-beat variation in the cardiac action potential duration is a phenomenon known as alter
223 -beat alternation (alternans) of the cardiac action potential duration is known to precipitate life-t
224  turnover of cardiac ion channels underlying action potential duration is regulated by ubiquitination
225 rdiomyocytes, which support the concept that action potential duration is uniform throughout the sarc
226 e Na(+) current (INaL), although it prolongs action potential duration, is not by itself sufficient t
227                                     Based on action potential duration, juxtacellular labeling, and i
228                                              Action potential duration, L-type Ca2+ current, and Na+
229                                              Action potential duration lengthening occurred during la
230 ong that RNF207 is an important regulator of action potential duration, likely via effects on HERG tr
231 on-recovery intervals (a surrogate for local action potential duration; median, 275 versus 241 ms; P=
232 F1473S to mexiletine paradoxically increased action potential duration, mimicking QT prolongation see
233 radients in the currents resulted in shorter action potential duration, minimum diastolic potential t
234 s activity, and showed a gradual decrease in action potential duration (n=23).
235 plateau phase and is thus a key regulator of action potential duration of cardiomyocytes.
236                                The composite action potential duration of heterogeneous tissue was we
237 d Kir2.1 expression, conduction velocity and action potential duration of the locally transduced and
238 f 2.5 Hz, and a variable prolongation of the action potential duration of up to several seconds.
239  both donor and failing hearts but shortened action potential duration only in failing hearts.
240  1/14 hearts at 100 nmol/L) without altering action potential duration or restitution and dispersion.
241                                              Action potential duration oscillations originate primari
242 essor of miR-1 and Ito, leading to prolonged action potential duration post myocardial infarction.
243 en minimal reductions in function can extend action potential duration, prolong QT intervals, and ult
244  model, acute interstitial edema exacerbated action potential duration prolongation and produced EADs
245 gical conditions quantitatively predicts the action potential duration prolongation caused by exposur
246  that the major ionic current change causing action potential duration prolongation in the presence o
247  syndrome (LQT9) and the cause of underlying action potential duration prolongation is incompletely u
248                                  Significant action potential duration prolongation was demonstrable
249 ing this fatal period manifested significant action potential duration prolongation, dispersion, and
250 n of RNF207 in zebrafish embryos resulted in action potential duration prolongation, occasionally a 2
251 epolarization dispersion caused by localized action potential duration prolongation.
252 sed late Na(+) current contribute equally to action potential duration prolongation.
253  despite similar left-ventricular monophasic-action-potential duration prolongations.
254 iques show a significant prolongation of the action potential duration prominently in late cardiac re
255 l approximated by an inverse sum of cellular action potential durations (R(2)=0.82).
256 ove 3 Hz, and cycle length dependence of the action potential duration, recapitulating key features o
257 ction potential and significantly reduce the action potential duration recorded in human cardiomyocyt
258 s reproducing changes in (dV(m)/dt)(max) and action potential duration required coupling to an HEK mo
259                                              Action potential duration restitution (APDR) and conduct
260       We hypothesize that apamin can flatten action potential duration restitution (APDR) curve and c
261 potential duration (APD), produced steepened action potential duration restitution (APDR) curves as w
262 ntly (p < 0.05) reduced the maximum slope of action potential duration restitution curve and converte
263                     The plateau phase of the action potential duration restitution curve steepened an
264 el was modified to reproduce rat ventricular action potential duration restitution to create reaction
265 ilure produced heterogeneous prolongation of action potential duration resulting in the decrease of t
266 g the effect of NE and ACh on rabbit cardiac action potential duration revealed that ACh blunted both
267                   During coverslip ischemia, action potential duration shortened, Ca(i) transient dur
268 ponses to ischemia-reperfusion, with greater action potential duration shortening (P<0.001 at 8-minut
269 tion of HMR-1556 mitigated S140G-IKs-induced action potential duration shortening and did not alter a
270 nnel blocker, counteracted adenosine-induced action potential duration shortening and prevented AF in
271 and, in Pcell, I(NaL) contributes additional action potential duration shortening at short cycle leng
272 AF-induced I(Ca,L) downregulation and in the action potential duration shortening that maintains the
273 embrane potential within and near the PZ and action potential duration shortening throughout the vent
274           TASK-1 channel inhibition prevents action potential duration shortening to maintain values
275  are responsible for the surprisingly modest action potential duration shortening.
276 potassium channels is enhanced, resulting in action potential duration shortening.
277                              Measurements of action potential duration show a significantly decreased
278          We have demonstrated that shortened action potential duration, slow conduction and triggered
279 sease, including prolongation of ventricular action potential duration, spontaneous early afterdepola
280 l mapping we observe increased dispersion of action potential duration, supersensitivity to beta-adre
281                                     We found action potential duration, systolic, and diastolic [Ca(2
282 reversed; however, females still have longer action potential durations than males.
283 s were assigned slower conduction and longer action potential durations than those for normal myocard
284  combine to synergistically increase cardiac action potential duration that is a likely cause of arrh
285  arrest is proarrhythmogenic by reducing the action potential duration through calcium channel inhibi
286 citability, slowed conduction, and prolonged action potential duration until 90% repolarization (APD9
287 e organization and evolution of alternans in action potential duration using high-resolution optical
288 ial effects of leptin involve restoration of action potential duration via normalization of transient
289      First, calcium transient duration minus action potential duration was longer at subendocardium i
290                                              Action potential duration was prolonged in N-cad CKO ven
291                                              Action potential duration was shorter in hetKO with IKto
292  sodium channel expression, I(Na) and atrial action potential duration were reduced and potassium cha
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

 
Page Top