ライフサイエンスコーパス: ventricular myocyte

1 ally detailed three-dimensional model of the ventricular myocyte.

2 ormal rapid activation and relaxation of the ventricular myocyte.

3 redictive in silico model of the adult human ventricular myocyte.

4 sing a physiologically detailed model of the ventricular myocyte.

5 onfirmed in a mathematical model of a rabbit ventricular myocyte.

6 rature-specific data-driven model of the rat ventricular myocyte.

7 handling, and ion currents were recorded in ventricular myocytes.

8 duction and Ca(2+)-wave generation in rabbit ventricular myocytes.

9 with Cav-3 was disrupted in the hypertrophic ventricular myocytes.

10 IKs amplitude in adult guinea pig and canine ventricular myocytes.

11 ns were complemented by experiments in mouse ventricular myocytes.

12 as many spontaneous Ca(2+) release events as ventricular myocytes.

13 ration in atrial and, to a lesser degree, in ventricular myocytes.

14 e not co-localized with mitochondria in live ventricular myocytes.

15 for the onset of bursting activity in mouse ventricular myocytes.

16 ocytes and acutely isolated adult guinea pig ventricular myocytes.

17 d Golgi PI4P depletion in neonatal and adult ventricular myocytes.

18 r measurements of cGMP in intact adult mouse ventricular myocytes.

19 for 50% and 90% repolarization in Trpm4(-/-) ventricular myocytes.

20 ion to in vitro model systems such as rodent ventricular myocytes.

21 and is localized in the nuclear membrane of ventricular myocytes.

22 expressed in enzymically isolated mammalian ventricular myocytes.

23 a2+ wave probability in field stimulated rat ventricular myocytes.

24 by IL-1beta was also seen in cultured adult ventricular myocytes.

25 NKA kinetics specific to guinea- pig and rat ventricular myocytes.

26 experiments with Ca waves using isolated rat ventricular myocytes.

27 disrupted intracellular Ca2+ homeostasis in ventricular myocytes.

28 coupling (ECC) is strikingly different from ventricular myocytes.

29 Rs are expressed and operative in human left ventricular myocytes.

30 ibrotic signaling in isolated murine primary ventricular myocytes.

31 its function as a repolarization reserve in ventricular myocytes.

32 as repolarization abnormalities in isolated ventricular myocytes.

33 2 AC isoforms in the regulation of ICa,L in ventricular myocytes.

34 NA binding activity in cultured neonatal rat ventricular myocytes.

35 eptors (RyRs) and caveolin-3 (CAV3) in mouse ventricular myocytes.

36 s to cell-wide SCWs in PLN-/-/RyR2-R4496C+/- ventricular myocytes.

37 ment of the L-type Ca(2+) current (ICa,L) in ventricular myocytes.

38 ct compartmentalization of these isoforms in ventricular myocytes.

39 model-predicted ChR2 behavior in guinea pig ventricular myocytes.

40 s in the elimination of Ito,f in KChIP2(-/-) ventricular myocytes.

41 cal for Akt-mediated NF-kappaB activation in ventricular myocytes.

42 .2 channels form clusters of varied sizes in ventricular myocytes.

43 nglia but no Na(V)1.8 expression in isolated ventricular myocytes.

44 equence) in primary cultures of neonatal rat ventricular myocytes.

45 cative of the increasing organization of the ventricular myocytes.

46 ve oxygen species generation in neonatal rat ventricular myocytes.

47 ncy of arrhythmogenic Ca(2+) fluctuations in ventricular myocytes.

48 ents in whole-cell patch-clamped rat cardiac ventricular myocytes.

49 ofibrillar proteins in isolated neonatal rat ventricular myocytes.

50 and pharmacological mechanisms in adult rat ventricular myocytes.

51 ion-based super-resolution microscopy in rat ventricular myocytes.

52 ase response to action potentials in mutated ventricular myocytes.

53 + waves during beta-AR stimulation in rabbit ventricular myocytes.

54 f calcium-handling genes and proteins in rat ventricular myocytes.

55 d to cultures of neonatal Sprague-Dawley rat ventricular myocytes.

56 (+)-K(+)-ATPase in membrane fragments and in ventricular myocytes.

57 eased L-type Ca(2+) current density in adult ventricular myocytes.

58 nce, and sodium current measured in isolated ventricular myocytes.

59 GF13 are the predominant FHFs in adult mouse ventricular myocytes.

60 Experiments were performed on rat ventricular myocytes.

61 of action potential morphology in guinea pig ventricular myocytes.

62 the amplitude of global Ca(2+) transients in ventricular myocytes.

63 ed SR membrane vesicles and in permeabilized ventricular myocytes.

64 (+) channel in the sarcolemma of adult mouse ventricular myocytes.

65 Quantify the 5 cardiac ARs in individual ventricular myocytes.

66 =110+/-3 mumol/L) and Na(+) current in mouse ventricular myocytes.

67 s the control of diastolic [Ca(2+) ]i in rat ventricular myocytes.

68 mputer simulations and experiments of rabbit ventricular myocytes.

69 re first tested by seeding with neonatal rat ventricular myocytes.

70 geneity that exists between atrial, VCS, and ventricular myocytes.

71 erformed using Fluo-3 in voltage clamped rat ventricular myocytes.

72 current, Ito, and IK,slow when compared with ventricular myocytes.

73 lly-detailed spatial Ca(2+) cycling model of ventricular myocytes.

74 [Ca(2+)]i with fluo-3 in voltage-clamped rat ventricular myocytes.

75 ains of nonfailing and failing human and rat ventricular myocytes.

76 the cardiac action potential and INa in rat ventricular myocytes.

77 isrupted intracellular Ca(2+) homeostasis in ventricular myocytes.

78 ers and its functional correlation in living ventricular myocytes.

79 2+) entry in control or STIM1 overexpressing ventricular myocytes.

80 chondria, both collected from adult rat left ventricular myocytes.

81 ata recorded from guinea pig isolated single ventricular myocytes.

82 n of GFP-RyR2 clusters was observed in fixed ventricular myocytes.

83 etween z-lines only at the periphery of live ventricular myocytes.

84 type Ca(2+) current (ICa, T) in hypertrophic ventricular myocytes.

85 kdown were examined in cultured neonatal rat ventricular myocytes.

86 How well can iPSC-CM model adult ventricular myocytes?

87 ated with the sarcoplasmic reticulum (SR) in ventricular myocytes; a median separation of 20 nm in 2D

88 NaK) densities were reduced in atrial versus ventricular myocytes according to experimental results.

89 ents in voltage clamped and field stimulated ventricular myocytes, along with mathematical modelling,

90 ogically detailed computational model of the ventricular myocyte and mathematical analysis.

91 were subsequently expressed in neonatal rat ventricular myocytes and acutely isolated adult guinea p

92 was confirmed to be present in neonatal rat ventricular myocytes and adult hearts.

93 rrhythmogenic-triggered activities in female ventricular myocytes and altered myocyte Ca2+ handling,

94 4 proteins are functionally present in mouse ventricular myocytes and are activated on Ca2+ -induced

95 ts encoding full-length Na(V)1.6 in isolated ventricular myocytes and confirmed the striated pattern

96 passing potassium ions outward to repolarize ventricular myocytes and end each beat.

97 We used permeabilized rat ventricular myocytes and fluorescently labeled DPc10, FK

98 luorescently tagged KCNQ1 and KCNE1 in adult ventricular myocytes and follow their biogenesis and tra

99 In neonatal rat ventricular myocytes and H9c2 myoblasts, ISO activated n

100 ypoxic regulation of Ca(V)1.2 in rat and cat ventricular myocytes and HEK-293 cells.

101 the mechanism of MANF release from cultured ventricular myocytes and HeLa cells, both of which secre

102 v3 coimmunoprecipitated with Kir2.1 in human ventricular myocytes and in heterologous expression syst

103 is-phosphorylated form in isolated adult rat ventricular myocytes and in mouse and rat ventricular my

104 voltage dependence of IH in Na/K pumps from ventricular myocytes and in ouabain-resistant pumps expr

105 luation, as well as decreasing the number of ventricular myocytes and inducing compensatory myocyte h

106 tial), and contractile force measurements in ventricular myocytes and intact cardiac muscles.

107 d refractoriness of calcium release in mouse ventricular myocytes and investigated how activation of

108 for the majority of PLA2 activity in rabbit ventricular myocytes and is responsible for arachidonic

109 lost its ability to support adhesion of rat ventricular myocytes and led to a significant reduction

110 Using adult rat ventricular myocytes and mouse-derived cardiac HL-1 card

111 We studied isolated R33Q and wild-type ventricular myocytes and observed properties not previou

112 ies of mitochondrial metabolism in the right ventricular myocytes and pulmonary vascular cells sugges

113 ed in Gq or by Gq expression in neonatal rat ventricular myocytes and reversed by CaMKIIdelta deletio

114 potent regulators of Na(+) channels in adult ventricular myocytes and suggest that loss-of-function m

115 We employed a co-culture of neonatal ventricular myocytes and sympathetic stellate neurons fr

116 also caused loss of T tubules in rat cardiac ventricular myocytes and the open canalicular system of

117 nofluorescence in freshly isolated adult rat ventricular myocytes and those in short-term primary cul

118 gical and Ca(2+)(i) dynamic abnormalities of ventricular myocytes and trabeculae from patients with H

119 DHHC5 coimmunoprecipitates with PLM in ventricular myocytes and transiently transfected cells.

120 gnalling augmented CaMKII activity in rabbit ventricular myocytes and, importantly, CaMKII activation

121 prevents the expansion of BMP signaling into ventricular myocytes, and ectopic activation of BMP mimi

122 hypertrophy in H9c2 cardiac cells, adult rat ventricular myocytes, and human induced pluripotent stem

123 IP3R function was determined in human left ventricular myocytes, and this analysis was integrated w

124 p to IKs amplitudes, in chronically stressed ventricular myocytes, and use COS-7 cell expression to p

125 d strands (n=152) in which host neonatal rat ventricular myocytes (AP duration=153.2+/-2.3 ms, conduc

126 Ventricular myocytes are excitable cells whose voltage t

127 The transverse (t-) tubules of mammalian ventricular myocytes are invaginations of the surface me

128 The dominant ventricular myocyte ARs present in all cells are the bet

129 tractility in the whole rat heart, adult rat ventricular myocytes (ARVMs), and myofibrils from both s

130 mplitude and SR Ca(2+) load in permeabilized ventricular myocytes as an endogenous cell biology model

131 ed with the opposite results in neonatal rat ventricular myocytes as p65 and p50 were decreased, and

132 rrent beyond steady state in voltage-clamped ventricular myocytes as reported by others.

133 ed sodium and potassium current densities in ventricular myocytes, as well as conduction slowing in t

134 166-selected cells are able to pace neonatal ventricular myocytes at a rate faster than their own.

135 We conducted experiments in rabbit ventricular myocytes at body temperature and found that

136 We show that the transfer of the adult ventricular myocyte (AVM) transcriptome into either a fi

137 estigated subpopulations of PLM in adult rat ventricular myocytes based on phosphorylation status.

138 o) during SR Ca(2+) release in intact rabbit ventricular myocytes by confocal microscopy.

139 cal microscopy and confirmed the findings in ventricular myocytes by directly observing fluorescently

140 tion of Ca(2+) spark refractoriness in mouse ventricular myocytes by examining how beta-adrenergic st

141 lation of Ca2+ spark refractoriness in mouse ventricular myocytes by examining how beta-adrenergic st

142 EADs were induced in isolated rabbit ventricular myocytes by exposure to 600 mumol l(-1) H(2)

143 erate hypokalaemia, increases Ca2+ levels in ventricular myocytes by reducing the pumping rate of the

144 d significant sarcomere shortening on murine ventricular myocytes compared to control.

145 iac myocyte and then experimentally in mouse ventricular myocytes, complemented by a theoretical agen

146 We developed a model for mouse ventricular myocyte contraction which is based on our pr

147 f variable sarcomere length into a model for ventricular myocyte contraction.

148 l pathway that constrains BMP signaling from ventricular myocytes, coordinates sarcomere assembly, an

149 In permeabilized ventricular myocytes, CPVT-CaMs at a physiological intra

150 PLCepsilon small interfering RNA (siRNA) in ventricular myocytes decreases endothelin-1 (ET-1)-depen

151 f GS-458967 on endogenous INaL in guinea pig ventricular myocytes demonstrate a robust concentration-

152 of this protocol in in vitro guinea-pig left-ventricular myocytes demonstrated that both voltage- and

153 hearts to VT/VF, patch clamped isolated SHR ventricular myocytes developed EADs and triggered activi

154 s and triggered activities in RyR2-R4496C+/- ventricular myocytes during sarcoplasmic reticulum Ca(2)

155 s characterized by a significant turnover of ventricular myocytes, ECs, and fibroblasts, physiologica

156 In ventricular myocytes, effects of SEA-0400 were tested on

157 The dyadic organization of ventricular myocytes ensures synchronized activation of

158 ics for CaM-RyR2 in normal and heart failure ventricular myocytes, estimate the percentage of Z-line-

159 triggered activity to the same extent as NR ventricular myocytes, except with larger EAD amplitude.

160 STAA ventricular myocytes exhibited arrhythmic contractions i

161 lated rabbit and rat hearts or patch-clamped ventricular myocytes exposed to hypokalemia (1.0-3.5 mmo

162 graftment of fibrin patches onto beating rat ventricular myocytes exposed to hypoxia showed an effect

163 isms leading to triggering of arrhythmias in ventricular myocytes exposed to low Ko.

164 RATIONALE: It is unknown whether every ventricular myocyte expresses all 5 of the cardiac adren

165 In permeabilized ventricular myocytes, FKBP12.6 and CaM colocalized to Z-

166 We show here that, in rat ventricular myocytes, fluorescent antibodies map the NBC

167 report prospective markers of atrial versus ventricular myocyte formation from hPSCs and their use i

168 recycling of the beta1-AR was determined in ventricular myocytes from AKAP5(-/-) mice.

169 Ventricular myocytes from cardiac-specific adult Scn1b n

170 Ventricular myocytes from cardiac-specific adult Scn1b n

171 um (Ca(2+)) and transverse-tubule imaging of ventricular myocytes from MCM-Speg(fl/fl) mice post HF r

172 Ventricular myocytes from mice heterozygous for the muta

173 INa and INa-L were measured in left ventricular myocytes from nonfailing, DHF, and CRT dogs.

174 HDAC5 phosphorylation and nuclear export in ventricular myocytes from the adult rat heart.

175 METHODS AND We studied ventricular myocytes from wild-type mice, mice with alph

176 ics of Ca(2+)-activated force development in ventricular myocytes from wild-type, but not those from

177 larly, Kv current density was 25% greater in ventricular myocytes from young adult males (P < 0.05).

178 production in fetal rat hearts and embryonic ventricular myocyte H9c2 cells via a selective increase

179 ion potentials in Wnt3a-treated neonatal rat ventricular myocytes had a lower upstroke amplitude (91

180 PC-1 was sufficient to trigger neonatal rat ventricular myocyte hypertrophy.

181 howed that GDF11 did not reduce neonatal rat ventricular myocytes hypertrophy, but instead induced hy

182 in suppressed L-type Ca(++) currents (rabbit ventricular myocytes, IC50=66.5+/-4 mumol/L) and IK1 (HE

183 acilitation of acid/base transporters in the ventricular myocyte, implying a specific role for the in

184 on suppressed Bnip3 levels and cell death of ventricular myocytes in response to hypoxia.

185 ents were recorded from isolated canine left ventricular myocytes in the presence of isoproterenol.

186 expression of STIM1 in cultured adult feline ventricular myocytes increased diastolic spark rate and

187 s of diabetes, spontaneous Ca(2+) release in ventricular myocytes increased ~5-fold.

188 Single-tilt tomograms of the dyads in rat ventricular myocytes indicated that type 2 ryanodine rec

189 ell death were recapitulated in neonatal rat ventricular myocytes infected with constitutively active

190 The transverse-tubule (T-tubule) system of ventricular myocytes is an important determinant of card

191 Contraction of ventricular myocytes is controlled by the terminal part

192 Intracellular calcium dynamics of ventricular myocytes isolated from KI hearts are altered

193 D We recorded Ca(2+) transients from cardiac ventricular myocytes isolated from rabbit hearts.

194 atically impaired in both the ventricles and ventricular myocytes isolated from RGS6(-/-) mice, and t

195 Confocal imaging of live ventricular myocytes isolated from the GFP-RyR2 mouse he

196 In this study, we used ventricular myocytes isolated from young (5-9 months) an

197 In adult mouse ventricular myocytes, it dose dependently increased sarc

198 In adult ventricular myocytes, KCNE1 maintains a stable presence

199 de that the absence of dystrophin in the mdx ventricular myocyte leads to impaired functional communi

200 hesis that targeted block of INaL would make ventricular myocytes less susceptible to small electrica

201 ac electrogenic Cl(-)/HCO3(-) transporter in ventricular myocytes, linking the critical roles of Slc2

202 Isolated patch-clamped rabbit ventricular myocytes loaded with Fluo-4 to image intrace

203 he first evidence that, in cultured neonatal ventricular myocytes, LPI triggers distinct signaling pa

204 d crest areas of the sarcolemma, whereas, in ventricular myocytes, LTCCs primarily cluster in T-tubul

205 (CA) enzymes, expressed at various sites in ventricular myocytes, may affect mitochondrial CO2 clear

206 ity changes of APs observed in a paced human ventricular myocyte model by decreasing and/or increasin

207 The formulations were applied to a ventricular myocyte model which has plasma-membrane Ca(2

208 In the adult rat ventricular myocyte model, both WT-Kv11.1 and T421M-Kv11

209 a pig myocytes, combined with a quantitative ventricular myocyte model, reveals a threshold behaviour

210 Using computer simulations of a ventricular myocyte model, we show that initiation and t

211 orporated this NCX model into an established ventricular myocyte model, which allowed us to predict r

212 345 ms was observed using the human cardiac ventricular myocyte model.

213 incorporated into a physiologically detailed ventricular myocyte model.

214 by performing a comprehensive analysis of 13 ventricular myocyte models.

215 r simulations using a realistic neonatal rat ventricular myocyte monolayer model provided crucial ins

216 Optical imaging in neonatal rat ventricular myocyte monolayers demonstrated slowed condu

217 ent protein (GFP) expression in neonatal rat ventricular myocyte monolayers.

218 rned cell pairs consisting of a neonatal rat ventricular myocyte (NRVM) coupled to an engineered huma

219 lectrophysiological property of neonatal rat ventricular myocyte (NRVM) cultures.

220 Treatment of confluent neonatal rat ventricular myocyte (NRVM) monolayers with astemizole or

221 system applied to monolayers of neonatal rat ventricular myocytes (NRVM).

222 beta-AR stimulation of neonatal rat ventricular myocytes (NRVMs) or cardiac fibroblasts with

223 silon protein was depleted from neonatal rat ventricular myocytes (NRVMs) using siRNA.

224 ranscription, HEK 293 cells and neonatal rat ventricular myocytes (NRVMs) were transfected with a luc

225 Using embryonic atrial and ventricular myocytes obtained from 4-day-old chick embry

226 (J(leak)) from the sarcoplasmic reticulum of ventricular myocytes occurs in spark and nonspark forms.

227 In ventricular myocytes of large mammals with low T-tubule

228 athematical models of Ca(2+) dynamics in the ventricular myocytes of the control, four-week, and seve

229 del, we engineered mutissues composed of two ventricular myocytes on deformable substrates of tunable

230 APs were recorded in rabbit ventricular myocytes paced at cycle lengths (CLs) decrea

231 al-time qPCR, echo- and electrocardiography, ventricular myocyte patch-clamp, coronary artery ligatio

232 In cultured adult feline ventricular myocytes, PKA inhibition protected myocytes

233 c models, we show that beta-catenin controls ventricular myocyte proliferation during development and

234 Our objective is to understand how adult ventricular myocytes regulate the IKs amplitudes under b

235 and the apoptotic response to doxorubicin in ventricular myocytes required RGS6-dependent ROS product

236 dent and -dependent mechanisms in atrial and ventricular myocytes, respectively.

237 AP recordings in rabbit ventricular myocytes revealed intermittent EADs, with sl

238 At the level of ventricular myocytes, Stim1 silencing or inhibition abro

239 patial localisation of [H(+)]i regulation in ventricular myocytes, suggesting that, by guarding pHi,

240 sonance energy transfer imaging of adult rat ventricular myocytes, surprisingly suggest that beta-blo

241 ription of the death gene Bnip3 resulting in ventricular myocyte survival.

242 aling and mTOR, the balance which determines ventricular myocyte survival.

243 We developed a model of the cardiac ventricular myocyte that simulates local stochastic Ca r

244 s and detailed mathematical models of rabbit ventricular myocytes that replicate the observed behavio

245 sed to develop models of isolated guinea pig ventricular myocytes that simulate the electrophysiologi

246 inculin (Vcl) plays a key structural role in ventricular myocytes that, when disrupted, can lead to c

247 In isolated rat ventricular myocytes, the CG digitoxin (DGT) increased t

248 In ventricular myocytes, the physiological function of stro

249 In isoproterenol-stimulated ventricular myocytes, the RyR2-A4860G mutation decreased

250 epending on initial ion circumstances within ventricular myocytes, these multi-stable AP states might

251 logy approach to test the hypothesis that in ventricular myocytes, these two apparently conflicting m

252 ed by the channel opener pinacidil in rabbit ventricular myocytes, through reducing the occurrence an

253 We developed an ionic model of the mouse ventricular myocyte to interrogate this potentially arrh

254 f V(m) in patterned cultures of neonatal rat ventricular myocytes to assess the relationship between

255 highly detailed mathematical model of mouse ventricular myocytes to disclose the key mechanisms unde

256 We used cultured neonatal rat ventricular myocytes to examine how chronic beta-AR stim

257 Exposing neonatal rat ventricular myocytes to hypo-osmotic medium resulted in

258 We subjected neonatal rat ventricular myocytes to mechanical stretch by exposing t

259 nged from minor alterations in anterior left ventricular myocytes to nearly complete loss of the t-sy

260 ies using phenylephrine-treated neonatal rat ventricular myocytes, to explore the putative antihypert

261 h factor 1 (IGF-1) treatment in neonatal rat ventricular myocytes, translocates to mitochondria and i

262 sting of monolayers of cultured neonatal rat ventricular myocytes treated with anthopleurin-A (AP-A).

263 in hERG-HEK cells as well as in neonatal rat ventricular myocytes treated with the muscarinic agonist

264 of intracellular Ca(2+) cycling dynamics in ventricular myocytes under periodic pacing have been dev

265 vestigated SERCA dimerization in rabbit left ventricular myocytes using a photoactivatable cross-link

266 ans were studied in single rabbit atrial and ventricular myocytes using combined [Ca(2+)]i and electr

267 Ca(2+) dynamics in intact and permeabilized ventricular myocytes using confocal microscopy.

268 ous Cav3 or Nedd4-2 in cultured neonatal rat ventricular myocytes using siRNA led to an increase in n

269 Ks was recorded from freshly isolated rabbit ventricular myocytes using whole-cell patch clamp.

270 um signals during wave propagation in rabbit ventricular myocytes, using high resolution fluorescence

271 s oocytes, and of native NKA isozymes in rat ventricular myocytes, using normal mammalian physiologic

272 properties and Ca(2+) cycling processes than ventricular myocytes (Vcell) and are frequently involved

273 bicin in the ventricles of mice and isolated ventricular myocytes via a posttranscriptional mechanism

274 voltage-clamp recordings from cGOF or icGOF ventricular myocytes (VM) show increased basal L-type Ca

275 more susceptible to Ca(2+) dysfunction than ventricular myocytes (VMs).

276 u is a phase of high resistance, which makes ventricular myocytes vulnerable to small electrical pert

277 stin using adenoviral vector in neonatal rat ventricular myocytes was associated with inhibition of A

278 all CA activity in the cytoplasm of isolated ventricular myocytes was found to be modest (2.7-fold ab

279 secretion of atrial natriuretic factor from ventricular myocytes was not increased by SR/ER calcium

280 +) and nitric oxide (NO) imaging in isolated ventricular myocytes was performed together with protein

281 or fluo-5N entrapped within the SR of rabbit ventricular myocytes, we addressed this controversy by d

282 In cultured neonatal rat ventricular myocytes, we compared the responses to IGF1

283 ) ([Ca(2+)]SR) decline during rest in rabbit ventricular myocytes, we found that approximately 76% of

284 Using rabbit ventricular myocytes, we show that this eigenvalue can b

285 between J(rel), I(Ca) and I(NCX) in porcine ventricular myocytes.We tested the hypothesis that durin

286 Isolated patch-clamped rabbit ventricular myocytes were exposed to either oxidative st

287 Furthermore, ventricular myocytes were found to be an important sourc

288 Adult ventricular myocytes were infected with adenoviruses exp

289 Isolated adult rat ventricular myocytes were infected with wild-type (WT)-K

290 ll shortening for epicardial and endocardial ventricular myocytes were investigated.

291 Ventricular myocytes were isolated from wildtype (C57Bl/

292 or GFP-expressing Cx43(+/+) (WT(GFP)) murine ventricular myocytes were patterned using microlithograp

293 Neonatal mouse ventricular myocytes were treated with a pathophysiologi

294 (2+)) alternans is a dynamical phenomenon in ventricular myocytes, which is linked to the genesis of

295 dings of action potentials on isolated mouse ventricular myocytes, which may contribute to the develo

296 rfusion or enzymatically digested to isolate ventricular myocytes, which were subsequently fixed at 0

297 aracterized by subcellular remodeling of the ventricular myocyte with a reduction in the scaffolding

298 Treatment of neonatal rat ventricular myocytes with either recombinant Wnt3a prote

299 ntify a new subpopulation of smaller working ventricular myocytes with more myosin.

300 Infection of 2D cultures of neonatal rat ventricular myocytes with WT and mutant channels increas