ライフサイエンスコーパス: APD

1 APD and APD adaptation were measured during an increase

2 APD decreased during the stressful parts of the film cli

3 APD depends on several preceding diastolic intervals (DI

4 APD in both LWHs and LANG hearts dropped steadily during

5 APD is less sensitive to changes in other IKr gating par

6 APD variations were associated with decreased transient

7 APDs also initiate blood digestion as components of mult

8 APDs have been considered as virulence factors of Trypan

9 roxysmal AF, and absent in controls (P=0.018 APD; P=0.042 spectral).

10 xperiments, while the model predicted 10.06% APD shortening with 29.33% block of INaL.

11 I(TO) subtraction) increased APD(50) by 31%, APD(90) by 17%, and APD(-61 mV) (reflecting cellular eff

12 th [1st, 3rd quartiles], 500 ms [500, 500]), APD alternans was detected in only 7 of 27 AF patients (

13 uM) caused a 28.67% block of INaL and 12.57% APD shortening in experiments, while the model predicted

14 on of intracellular Ca(2+) release abolished APD alternans, indicating that [Ca(2+)]i dynamics have a

15 By adapting APD-AED method in the case of UAE, the intensive optimum

16 using carbenoxolone only minimally affected APD distribution in confluent cells.

17 itive to inactivation shifts, which affected APD and SD1 concordantly; (4) activation shifts of the s

18 Q-T interval of the electrocardiogram alter APD stability, and modulate responsiveness to pharmacolo

19 We hypothesized (1) that CRT may alter APD and (2) that the effect of CRT on APD may be differe

20 ate control (LMC) or LQT1 myocytes, although APDs were also prolonged in LMC myocytes and LQT1 myocyt

21 An APD profile at 75 percent repolarization with a 16.6 +/-

22 The internal gain of an APD can improve system signal-to-noise ratio (SNR).

23 ncreased APD(50) by 31%, APD(90) by 17%, and APD(-61 mV) (reflecting cellular effective refractory pe

24 the pacing threshold for both SR Ca(2+) and APD alternans (188+/-15 and 173+/-12 ms; P<0.05 versus b

25 concordant but not discordant SR Ca(2+) and APD alternans.

26 Results show that LV/RV APD and APD adaptation heterogeneities promote unidirectional bl

27 APD and APD adaptation were measured during an increase in heart

28 an vernakalant, which increased both APD and APD dispersion.

29 /RV junction, LV/RV heterogeneity in APD and APD rate adaptation promotes reentrant activity and its

30 covered DYS and nNOS, and normalised APD and APD rate-dependency.

31 nation of fibrillation by modulating APD and APD/conduction velocity restitution slopes in atrial tis

32 ences in action potential duration (APD) and APD rate adaptation and their contribution to arrhythmog

33 3 ms and 93+/-6 versus 76+/-4 ms for CaT and APD alternans, respectively, P<0.05), suggesting increas

34 racted great attention for monitoring DA and APD levels but none of the methods developed so far aime

35 AF is linked to atrial APD heterogeneity and APD reduction due to progressive remodelling.

36 tations produced distinct effects on IK1 and APD shortening.

37 INa-L block with lidocaine shortened QTc and APD more at 6.5 hours than at 50 minutes (QTc) or 30 min

38 Dofetilide monotonically increased QTc and APD throughout 6.5-hour exposure.

39 The large differences in theta' and APD restitution contrasted with minor differences in max

40 PDs in LWHs were longer at all workloads and APD reductions during deoxygenation were blunted in both

41 eral preceding diastolic intervals (DIs) and APDs, which complicates the prediction of alternans.

42 egrees offcut from the [110] do not show any APDs, whereas samples grown on the exactly oriented subs

43 that hMSCs dose-dependently increased APD90, APD dispersion, inducibility of re-entry and affected sp

44 the KCNQ1 S140G mutation abbreviated atrial APD and ERP and flattened APD and ERP restitution curves

45 ed electrical remodelling abbreviated atrial APD non-uniformly across the atria; this resulted in rel

46 i-arrhythmic strategies that increase atrial APD without increasing its dispersion are effective in t

47 Amiodarone increased atrial APD and reduced APD heterogeneity and was more effective

48 gene deletion or inhibition shortened atrial APD and increased atrial fibrillation inducibility in vi

49 stenance of rotors in AF is linked to atrial APD heterogeneity and APD reduction due to progressive r

50 ested the ability of lurasidone, an atypical APD with potent 5-HT(1A) partial agonist properties, tan

51 sidone, as well as the prototypical atypical APD clozapine, restored NMDAR-mediated synaptic response

52 The typical and atypical APDs do not differ in improving psychopathology in non-T

53 operties of a series of typical and atypical APDs in a novel time-resolved fluorescence resonance ene

54 ributes to cognitive enhancement by atypical APDs in patients with schizophrenia.

55 tively correlated in SZ patients on atypical APDs and in NCs; this correlation was stronger in SZ pat

56 tively correlated in SZ patients on atypical APDs; this correlation was significantly stronger than t

57 Overall, choosing among the atypical APDs as first-line treatment represents the best course

58 Clozapine is unique among the atypical APDs in its efficacy for ameliorating psychosis in patie

59 Cognitive benefits of the atypical APDs may be superior for some domains of cognition and r

60 differ in mechanism of action, with atypical APDs providing important modulation of serotonergic neur

61 ation is negatively correlated with baseline APD and positively correlated with PCL.

62 ng AF than vernakalant, which increased both APD and APD dispersion.

63 tween normal and SZ cases, nor influenced by APD, in any region tested.

64 Alternans was measured by APD and spectral analysis.

65 longer detect any anti-Dsg3 clones in PV1 by APD.

66 pparent increase in Kv3.1b protein levels by APDs in SZ neocortex was confirmed in laboratory rodents

67 SZ neocortex, a deficit that is restored by APDs.

68 ion alterations that are sufficient to cause APD prolongation and EADs, the predominant characteristi

69 ) within the mammalian myocardium can change APD and the Q-T interval of the electrocardiogram alter

70 Apamin did not change APD(80) in normal ventricles, but prolonged APD(80) in f

71 nated reentry by prolonging APD and changing APD and conduction velocity restitution slopes, thereby

72 tion on pacing history and tau characterizes APD accommodation, which is an exponential change of APD

73 nterior cingulate cortex (ACC) after chronic APD treatment, regardless of the APD administered.

74 egion-specific structural effects of chronic APD treatment on the rat cortex, primarily but not exclu

75 etric findings and demonstrated that chronic APD treatment had no effect on the total number of neuro

76 d in laboratory rodents treated with chronic APDs.

77 antagonist to the development of concordant APD alternans.

78 n on the exactly oriented substrates contain APDs.

79 zophrenia and related disorders than current APDs.

80 With JNJ-303, ISO decreased APD significantly more in the epicardium as compared to

81 ty, postoperative afferent pupillary defect (APD), old age, scleral laceration, and retinal detachmen

82 d power density and absorbed energy density (APD-AED) and response surface methodology (RSM).

83 f patients on automated peritoneal dialysis (APD) is increasing worldwide and may be guided by clinic

84 able states consisting of APs with different APDs, and caused multiple hysteretic dynamics.

85 ontrast, continuous ISO perfusion diminished APD prolongation and reduced the incidence of EADs in LQ

86 APD heterogeneity and converting discordant APD alternans to concordant ones.

87 IgG(+) repertoire by antibody phage display (APD) and PCR indicated that six clonal lines persisted i

88 characterise and quantify antiphase domains (APDs) in GaP thin films grown on different (001) Si subs

89 ut only in cases without antipsychotic drug (APD) treatment; Kv3.1 levels are normal in antipsychotic

90 hanisms of action of the antipsychotic drug (APD), clozapine, is of great importance, as clozapine is

91 newly approved atypical antipsychotic drug (APD), on NMDAR synaptic function in rat frontal cortical

92 evidence suggests that antipsychotic drugs (APD) might affect brain structure directly, particularly

93 Antipsychotic drugs (APDs) are best classified as typical or atypical.

94 Atypical antipsychotic drugs (APDs) have been hypothesized to show reduced extrapyrami

95 Current antipsychotic drugs (APDs) show efficacy with positive symptoms, but are limi

96 All FDA-approved antipsychotic drugs (APDs) target primarily dopamine D2 or serotonin (5-HT2A)

97 ed hippocampal neurons, antipsychotic drugs (APDs) were proposed to accumulate in synaptic vesicles b

98 treatment with atypical antipsychotic drugs (APDs), which are serotonin (5-HT)(2A)/dopamine D(2) anta

99 lopment of new atypical antipsychotic drugs (APDs), with better tolerability due to more selective do

100 ith typical or atypical antipsychotic drugs (APDs).

101 tive I(TO) changes on AP shape and duration (APD), and on afterdepolarisations or abnormal automatici

102 d as the changes of AP profile, AP duration (APD) and its dispersion across the atria, and the vulner

103 were quantified on AP profile, AP duration (APD) restitution, effective refractory period (ERP) rest

104 (TOLB) to identify the level of AP duration (APD) shortening attributed to KATP channel activation.

105 ependent changes in ventricular AP duration (APD), and variations in APD at a fixed heart rate are bo

106 showed gradual prolongation of AP duration (APD), and were annihilated without AP configuration chan

107 Effects of mutations on AP duration (APD), conduction velocity (CV), effective refractory per

108 the cardiac action potential (AP) duration (APD) is a well-known arrhythmogenic mechanism.

109 t changes in action potential (AP) duration (APD), which may be subtle.

110 SR Ca(2+) and action potential duration (APD) alternans occurred in-phase, but SR Ca(2+) alternan

111 t (kiCa) produced action potential duration (APD) alternans seen clinically at slower pacing rates.

112 haracteristics of action potential duration (APD) alternans were investigated.

113 (restitution) in action potential duration (APD) and activation latency are central targets for clin

114 RV differences in action potential duration (APD) and APD rate adaptation and their contribution to a

115 Na-L) prolong the action potential duration (APD) and contribute to early afterdepolarizations.

116 ulting changes in action potential duration (APD) and its short term variability (SD1) were measured.

117 such as decreased action potential duration (APD) and plateau height-were found when hCMs were couple

118 d chromatography; action potential duration (APD) and rate dependent adaptation were assessed by sing

119 olongation of the action potential duration (APD) at 50% and 90% repolarization in UNx EPI cardiomyoc

120 pping techniques, action potential duration (APD) at 80% of repolarization was longer in CKD rats (78

121 rmined transmural action potential duration (APD) before and after 100 nmol/L apamin administration i

122 that CO prolongs action potential duration (APD) by inhibiting a subset of inward-rectifying potassi

123 t prolongation of action potential duration (APD) can be further enhanced by lowering extracellular p

124 responding longer action potential duration (APD) in cardiomyocytes incubated with L5 in vitro.

125 ge on ventricular action potential duration (APD) in conscious healthy humans has not been reported.

126 n groups, because action potential duration (APD) in T2DM failed to undergo progressive adaptation to

127 d prolongation of action potential duration (APD) in TAC and leptin-treated sham animals, whereas, fo

128 ial dispersion of action potential duration (APD) is a substrate for the maintenance of cardiac fibri

129 ich regulates the action potential duration (APD) of individual myocytes and thus the QT interval by

130 lternation in the action potential duration (APD) of myocytes, i.e. alternans, is believed to be a di

131 gs (shortens) the action potential duration (APD) of that beat.

132 erved substantial action potential duration (APD) prolongation and prominent early afterdepolarizatio

133 re is ventricular action potential duration (APD) prolongation.

134 (AP) morphology, action potential duration (APD) restitution and conduction velocity (CV) restitutio

135 the slope of the action potential duration (APD) restitution curve, by reducing the propensity of AP

136 ole in post-shock action potential duration (APD) shortening and recurrent spontaneous ventricular fi

137 tilide effects on action potential duration (APD) were studied in canine left ventricular subendocard

138 s in contraction, action potential duration (APD), and magnitude of the Ca(2+) transient (CaT).

139 utation prolonged action potential duration (APD), produced steepened action potential duration resti

140 ng alternation in action potential duration (APD), which is considered to be a precursor of ventricul

141 normal changes in action potential duration (APD).

142 RG) and shortened action-potential duration (APD).

143 heterogeneity of action potential duration (APD).

144 ural gradients of action potential duration (APD).

145 dent reduction in action potential duration (APD).

146 rtiapin prolonged action potential duration (APD; 54.7+/-24.0 to 128.8+/-16.9 milliseconds; P<0.0001)

147 Action potential durations (APD(50,75,90)), effective refractory period (ERP), post

148 on latencies and action potential durations (APDs) from monophasic action potential recordings were u

149 ffects of VIP on action potential durations (APDs) in isolated canine left atria.

150 used to measure action potential durations (APDs) in the presence of the IKs blocker JNJ-303 and the

151 related with alternans magnitude than either APD or theta restitution gradient.

152 nans is Ca(2+) -driven, electromechanically (APD-Ca(2+) ) concordant alternans becomes electromechani

153 is synaptic corelease is expected to enhance APD antagonism of D2Rs where and when dopaminergic trans

154 n patients with heart failure, LV epicardial APD (activation recovery interval) altered during CRT.

155 In current-clamp experiments, APD and CaT alternans strongly correlated in time and ma

156 Fitting APD with a function of two previous APDs and CLs permitt

157 abbreviated atrial APD and ERP and flattened APD and ERP restitution curves.

158 rom unipolar electrograms as a surrogate for APD (n=19) were recorded from right and left ventricular

159 ation recovery intervals, as a surrogate for APD, were measured from the LV epicardium in 13 patients

160 ns of the extraction, i.e. 70% EtOH, 30mL/g, APD of 0.22W/mL, AED of 450J/mL are able to achieve simi

161 ditions of MAE obtained at 80% EtOH, 50mL/g, APD of 0.35W/mL, AED of 250J/mL can be used to determine

162 current (I(Kr)) density, served to generate APD dispersion, high-frequency rotor formation, wavebrea

163 ed 3,901 patients of which 1,819 (46.6%) had APD as their first modality.

164 operty, resulting in rapid and heterogeneous APD shortening.

165 However, if APD accommodation is small (tau </= 250 ms), increase in

166 cross-correlation based approaches to image APDs.

167 ncrease arrhythmias rely on small changes in APD and Q-T intervals as criteria for safety pharmacolog

168 A 20% decrease in APD dispersion by Type C hMSCs compared to hEAG1-active

169 esults suggest that LV/RV heterogeneities in APD adaptation cause a transient increase in APD dispers

170 t the LV/RV junction, LV/RV heterogeneity in APD and APD rate adaptation promotes reentrant activity

171 APD adaptation cause a transient increase in APD dispersion in the human ventricles following rate ac

172 or type 2 diabetes exhibited an increase in APD that was reversed by expression of constitutively ac

173 The increases in APD and INaP in myocytes translated into QT interval pro

174 ricular AP duration (APD), and variations in APD at a fixed heart rate are both reliable biomarkers o

175 ng kinetics at the D2 receptor may result in APDs with improved therapeutic profile.Atypical antipsyc

176 with hMSC-derived exosomes did not increase APD in neonatal rat cardiomyocyte cultures.

177 We found that JNJ-303 alone did not increase APD.

178 , which led to decreased IhERG and increased APD.

179 nd additional E-4031 significantly increased APD.

180 TO) block (100% I(TO) subtraction) increased APD(50) by 31%, APD(90) by 17%, and APD(-61 mV) (reflect

181 on channels, VIP shortens APD with increased APD spatial heterogeneity and decreases intra-atrial con

182 iarrhythmic effect is hampered by increasing APD variance.

183 Pacing-induced APD and CaT alternans were studied in single rabbit atri

184 a'), action potential wavelengths (lambda' = APD x theta'), and their corresponding alternans depende

185 For the case of large APD accommodation (tau >/= 290 ms), increase in alpha le

186 ysis of in vivo electrograms revealed longer APD in LV than RV (207.8 +/- 21.5 vs 196.7 +/- 20.1 ms;

187 ing phase 4 depolarization (n=19) had longer APDs, smaller amplitude and V(max), and a more positive

188 Because many APDs are dopamine (DA) D2 receptor (D2R) antagonists, su

189 cyclase, a recent study has shown that many APDs affect not only G(i/o)- but they can also influence

190 ours than at 50 minutes (QTc) or 30 minutes (APD) dofetilide administration.

191 nd termination of fibrillation by modulating APD and APD/conduction velocity restitution slopes in at

192 ata indicate that parasites express multiple APD isoenzymes of various functions that can now be spec

193 ation recovered DYS and nNOS, and normalised APD and APD rate-dependency.

194 ally discordant SR Ca(2+) alternans, but not APD alternans, the pacing threshold for discordance, or

195 reening where competitive binding of a novel APD and DA to a dopamine D3 receptor (D3R) was investiga

196 mmodation, which is an exponential change of APD over time once basic cycle length (BCL) changes.

197 ac stability, as manifested by the degree of APD alternans.

198 he computational model to test the degree of APD prolongation induced by small electrical perturbatio

199 ers characterizing whether the dependence of APD on previous DIs or CLs is strong (typical for voltag

200 Here, alpha quantifies the dependence of APD restitution on pacing history and tau characterizes

201 ges to tissue excitability and dispersion of APD in mutation conditions.

202 more, VIP increased spatial heterogeneity of APD and conduction velocity, as assessed by the SDs of A

203 ation, such as shortening of APD and loss of APD rate-dependency, but had no effect in patients with

204 The percentages of APD prolongation in the last 4 hearts at 2000 ms PCL aft

205 slopes, thereby altering the probability of APD alternans and rotor destabilization.

206 ignificant), but significant prolongation of APD(50) at 30 mumol/L and rapid rates.

207 t caused variable but slight prolongation of APD(90) (P=not significant), but significant prolongatio

208 ol by reverse rate-dependent prolongation of APD(90) and ERP.

209 - and reverse rate-dependent prolongation of APD(90).

210 itution curve, by reducing the propensity of APD alternans, converting discordant to concordant alter

211 nduction velocity, as assessed by the SDs of APD and conduction velocity, and atrial fibrillation ind

212 y atrial fibrillation, such as shortening of APD and loss of APD rate-dependency, but had no effect i

213 id and spatially heterogeneous shortening of APD preceded the onset of arrhythmias in T2DM.

214 Limiting the use of APD in disadvantaged population may be unethical.

215 which we can further assess the potential of APDs as targets for novel effective intervention strateg

216 oup divided by treatment response or type of APDs.

217 The effect of mental challenge on APD was not secondary to emotionally induced altered res

218 alter APD and (2) that the effect of CRT on APD may be different in patients who exhibit a good hemo

219 SD1 more than expected by its dependency on APD; (2) mIKr completely reversed APD and SD1 changes ca

220 The effect on APD was opposite in patients showing a good hemodynamic

221 L are sufficient to reproduce the effects on APD observed in DHF and CRT myocytes.

222 of the same magnitude had marginal impact on APD, but only when reducing mIKr, they significantly inc

223 interest was the probability to start PD on APD.

224 However, the effect of reverse remodeling on APD during cardiac resynchronization therapy (CRT) has n

225 le modulating role of altered respiration on APD, the subjects then repeated the same breathing patte

226 an American patients less likely to start on APD (Odds ratio 0.74 CI95% 0.58-0.94) compared to Whites

227 cational levels were more likely to start on APD (Odds ratio 3.70, CI95% 2.25-6.09) compared to illit

228 length thresholds to induce CaT alternans or APD alternans were longer in CKD rats than normal rats (

229 of psychiatric disorders compared with other APDs.

230 At 50% perfusate oxygenation, APD and LVDP were significantly higher in LWHs perfused

231 At rapid pacing, APD maps show areas of conduction block in the failing h

232 ion of aspartic cathepsin D-like peptidases (APDs) has been often discussed as an antiparasite interv

233 The percent APD prolongation is negatively correlated with baseline

234 Avalanche photodiodes (APDs) are essential components in quantum key distributi

235 endence of the DI on the immediate preceding APD (i.e. feedback).

236 Fitting APD with a function of two previous APDs and CLs permitted us to estimate lambdaalt along wi

237 Ca2+ homeostasis which drives proarrhythmic APD alternans in patients with AF.

238 Apamin prolonged APD from 363 ms (95% confidence interval [CI], 341-385)

239 APD(80) in normal ventricles, but prolonged APD(80) in failing ventricles at either long (>/=300 ms)

240 hosphoinositide 3-kinase and INa-L prolonged APD acutely but no additional prolongation occurred on c

241 Isoprenaline (ISO) prolonged APDs and triggered EADs in LQT1 myocytes in the presence

242 ) prevented/terminated reentry by prolonging APD and changing APD and conduction velocity restitution

243 evated the plateau, significantly prolonging APD, in both species.

244 Apamin prolongs APD at long and short, but not at intermediate pacing cy

245 hibition of Kir2.2 and Kir2.3 by CO prolongs APD in myocytes, cardiac Kir2.2 and Kir2.3 are promising

246 We were able to image and quantify APDs by relating the asymmetrical intensity distribution

247 Amiodarone increased atrial APD and reduced APD heterogeneity and was more effective in terminating

248 P)3.1 channel inhibition reverses AF-related APD shortening.

249 endency on APD; (2) mIKr completely reversed APD and SD1 changes caused by IKr blockade; (3) repolari

250 During sinus rhythm, APD was shorter in LWHs compared to LANG hearts.

251 Results show that LV/RV APD and APD adaptation heterogeneities promote unidirect

252 Following rate acceleration, LV/RV APD dispersion experienced an increase of up to 91% in 1

253 the methods developed so far aimed to screen APD candidates.

254 the atria; this resulted in relatively short APDs co-existing with marked regional differences in the

255 duces regionally heterogeneous and shortened APD; these respectively facilitate initiation and mainte

256 Lidocaine shortened APD equally during acute and chronic moxifloxacin superf

257 Regional hERG overexpression shortened APD and increased rotor incidence in the hERG overexpres

258 VIP shortened APD and slowed conduction velocity in a dose-dependent m

259 iac resynchronization therapy (CRT) shortens APD compared with dyssynchronous heart failure (DHF); ho

260 iverse effects on ion channels, VIP shortens APD with increased APD spatial heterogeneity and decreas

261 .5 vs 196.7 +/- 20.1 ms; P<0.05), and slower APD adaptation in LV than RV (time constant tau(s) =47.0

262 We investigated the role played by spatial APD dispersion in fibrillatory dynamics.

263 ntiarrhythmic effect by reducing the spatial APD heterogeneity and converting discordant APD alternan

264 r level into the mechanisms by which spatial APD dispersion contributes to wavebreak, rotor stabiliza

265 However, the steep APD gradient at the border zone proved to be the primary

266 In controls, no intervention steepened APD restitution or initiated AF.

267 deling revealed that isoproterenol steepened APD restitution by increased L-type calcium current and

268 inactivation, whereas rapid pacing steepened APD restitution via increased cardiac inward potassium r

269 Therefore, in the striatum, APDs are released with DA in response to action potentia

270 al index of individual propensity to AF than APD alternans.

271 SD1 may be more sensitive than APD in detecting IKr-dependent repolarization abnormalit

272 The APD prolongation was mediated by an increase of L-type c

273 d regional increase in I(Kr) abbreviated the APD and hyperpolarized the resting potential.

274 DHF-induced enhanced INa-L, abbreviated the APD, and suppressed early afterdepolarizations.

275 suppression of INa-L, thus, abbreviating the APD and reducing the frequency of early afterdepolarizat

276 onlinear functional relationship between the APD and the preceding diastolic interval (DI).

277 lop a mathematical framework to describe the APD signal using an autoregressive stochastic model, and

278 Here, the APD cyamemazine (CYAM) is visualized directly by two-pho

279 ting with marked regional differences in the APD at junctions of the crista terminalis/pectinate musc

280 ter chronic APD treatment, regardless of the APD administered.

281 , whereas, following TAC, leptin reduced the APD towards control values.

282 ints during repolarisation revealed that the APD(90) increase resulted mainly from plateau-elevation,

283 serve attenuation might be attributed to the APD variability caused by multi-stability in cardiac AP

284 Monitoring of these APD candidates in biological fluids is of great importan

285 m-selective K(2P)3.1 currents contributes to APD shortening in patients with chronic AF, and K(2P)3.1

286 s a paradoxical resistance of T2DM hearts to APD adaptation.

287 y diastolic [Ca(2+)]SR alternans and lead to APD alternans.

288 Exposure to APDs early in development causes dose-dependent developm

289 ons of SZ and in the therapeutic response to APDs.

290 With TOLB, APDs in LWHs were longer at all workloads and APD reduct

291 )/dopamine D(2) antagonists, but not typical APDs, eg, haloperidol, reverses the PCP-induced NOR defi

292 can be minimized by limiting use of typical APDs.

293 stronger than that in SZ patients on typical APDs or in NCs.

294 SZ patients on atypical rather than typical APDs or in NCs.

295 f a mental challenge protocol on ventricular APD in conscious humans.

296 fects of GS-458967 on guinea pig ventricular APD.

297 n a disturbance of Ca(2+) signaling, whereas APD alternans are a secondary consequence, mediated by C

298 ia and most likely other disorders for which APDs are used.

299 with the PCL, but negatively correlated with APD when PCL is fixed.

300 nce imaging in rats treated chronically with APDs, we used automated analysis techniques to map the r