ライフサイエンスコーパス: cerebral artery

1 yer 2/3 located just posterior to the middle cerebral artery.

2 any level of the internal carotid or middle cerebral artery.

3 via endovascular perforation of the anterior cerebral artery.

4 with changes in flow velocity in the middle cerebral artery.

5 ebral artery: anterior, middle, or posterior cerebral artery.

6 us transient outward currents (STOCs) in rat cerebral arteries.

7 functional significance in myocytes of small cerebral arteries.

8 e primary sensor of intraluminal pressure in cerebral arteries.

9 us transient outward currents (STOCs) in rat cerebral arteries.

10 nd occlusion or high-grade stenosis in major cerebral arteries.

11 by vasculopathy of the small and medium-size cerebral arteries.

12 th occlusion or high-grade stenosis in major cerebral arteries.

13 ron pathway may promote virus persistence in cerebral arteries.

14 tic plaques in the aortic arch, cervical, or cerebral arteries.

15 voked constriction of pressurized rat middle cerebral arteries.

16 ilated the rat and C57BL/6 mouse pressurized cerebral arteries.

17 change in the mechanical properties of mouse cerebral arteries.

18 nching at bifurcations of the major proximal cerebral arteries.

19 asoconstriction and structural remodeling of cerebral arteries.

20 ng the hemodynamics characteristics of major cerebral arteries.

21 associated with hypercontractility of intact cerebral arteries.

22 d into the NO-sensitive compartment of small cerebral arteries.

23 t adhesion under flow in structurally intact cerebral arteries.

24 bral artery myocytes and vasoconstriction of cerebral arteries.

25 currents to induce myogenic constriction of cerebral arteries.

26 ery (39 vs 109 cm3; P = .004), and M2 middle cerebral artery (33 vs 59 cm3; P = .04) occlusions.

27 erminus (75 vs 190 cm3; P < .001), M1 middle cerebral artery (39 vs 109 cm3; P = .004), and M2 middle

28 the internal carotid artery (ICA), anterior cerebral artery (ACA), and / or middle cerebral artery (

29 rophic inward remodelling within the largest cerebral artery after high-thoracic SCI, leading to incr

30 vasospasm was 4 days (+/- 2 d) in the middle cerebral arteries and 5 days (+/- 2.5 d) in the basilar

31 ximately 30-fold higher than AT1 Ra in whole cerebral arteries and approximately 45-fold higher in is

32 Changes of middle cerebral arteries and basilar arteries were extremely ra

33 amyloid beta peptide (Abeta) within walls of cerebral arteries and is an important cause of intracere

34 abled by a dynamic association with PSD95 in cerebral arteries and suggest that a disruption of such

35 ive smooth muscle cells (SMCs) isolated from cerebral arteries and that acute knockdown diminishes th

36 elocities (transcranial Doppler) from middle cerebral artery and blood pressure (Finometer) were reco

37 occlusion of the internal carotid or middle cerebral artery and evidence of salvageable brain tissue

38 rom patients with an occlusion in the middle cerebral artery and from an additional cohort of patient

39 arcts in the anterior cerebral artery-middle cerebral artery and middle cerebral artery-posterior cer

40 anial aneurysms of the right and left middle cerebral artery and right internal carotid artery.

41 into a mixed supply from both the posterior cerebral artery and the anterior choroidal artery or a s

42 internal carotid artery [ICA] with M1 middle cerebral artery and/or A1 anterior cerebral artery invol

43 approximately 30-fold greater than AT1 Ra in cerebral arteries, and knockdown of AT1 Rb selectively d

44 roscopy, blood flow velocities of the middle cerebral artery, and cardiac output at baseline, 5 minut

45 t strokes are caused by occlusion of a major cerebral artery, and substantial advances have been made

46 Three months later the right middle cerebral artery aneurysm was embolised and the woman was

47 ascular treatment of small unruptured middle cerebral artery aneurysms is feasible and effective.

48 ariants of internal carotid artery, anterior cerebral artery, anterior communicating artery, middle c

49 50%) stenosis or occlusion of a single large cerebral artery: anterior, middle, or posterior cerebral

50 al growth, kidney volumes, and umbilical and cerebral artery blood flow (median gestational age of 30

51 Beat-by-beat measurements of middle cerebral artery blood flow velocity (MCAv; transcranial

52 Mean middle cerebral artery blood velocity (MCA V(mean)), mean arter

53 ovascular control were measured using middle cerebral artery blood velocity (MCAv(mean) ) and its rea

54 xy causing compression of bilateral anterior cerebral artery branches and leading to bilateral caudat

55 e profound effect on endothelial function in cerebral arteries compared with skeletal muscle feed art

56 red by near-infrared spectroscopy and middle cerebral artery Doppler.Measurements and Main Results: F

57 rtant to reduce disease risk associated with cerebral artery dysfunction in conditions such as advanc

58 Greater large artery stiffness can cause cerebral artery endothelial dysfunction by reducing NO b

59 The mechanisms for impaired cerebral artery endothelial function are reduced nitric

60 greater large artery stiffness have impaired cerebral artery endothelial function, but generally pres

61 in kinase A substrate antibody revealed that cerebral arteries exposed to KV1-C peptide showed marked

62 Bilateral transcranial middle cerebral artery flow velocities using Doppler and jugula

63 rents in smooth muscle cells and constricted cerebral arteries from both groups.

64 d blocked stretch-induced cation currents in cerebral arteries from both groups.

65 Isolated cerebral arteries from HA fetuses showed a higher contra

66 can cause compression of bilateral anterior cerebral arteries from the expanding mass and lead to bi

67 CADASIL, an inherited SVD, alters cerebral artery function, compromising blood flow to the

68 n C (L68Q) readily forms amyloid deposits in cerebral arteries in affected individuals resulting in e

69 ET-1-mediated vasoconstriction of the middle cerebral artery in a rat model.

70 n 2010 and 2018 with occlusion of the middle cerebral artery in the M1-/proximal M2-segment or termin

71 angio-CT revealed an aneurysm of the middle cerebral artery, in its distal branch.

72 In smooth muscle cells from cerebral arteries, increasing intraluminal pressure enga

73 Key experiments on human cerebral arteries indicate that CaV3.2 is present and dr

74 eases in intraluminal pressure of cannulated cerebral arteries induced myogenic constriction and conc

75 d parietal cortex is common following middle cerebral artery infarction, leading to upper extremity p

76 ears; range, 61 to 82) with malignant middle-cerebral-artery infarction to either conservative treatm

77 complete or subtotal space-occupying middle-cerebral-artery infarction.

78 ears of age or older with a malignant middle-cerebral-artery infarction.

79 ddle cerebral artery vs M2 segment of middle cerebral artery), intravenous alteplase (yes vs no), bas

80 M1 middle cerebral artery and/or A1 anterior cerebral artery involvement) or tandem (extracranial or

81 wever, which neurons control the dynamics of cerebral arteries is not well understood.

82 The anterior cerebral artery is a common location of intracranial ane

83 o 83 years, with confirmed first-time middle cerebral artery ischemic stroke with modified Rankin sca

84 stroke volume after femoral artery or middle cerebral artery ligation, respectively.

85 or endovascular treatment of the left middle cerebral artery (LMCA) aneurysm because it posed the gre

86 interval [CI]: 1.1, 2.8; P = .02) and middle cerebral artery location (OR, 1.9; 95% CI: 1.2, 3.0; P =

87 mboembolic events were female sex and middle cerebral artery location.

88 ranial internal carotid artery and/or middle cerebral artery M1 and/or M2) on computed tomographic an

89 stroke induction by occlusion of the middle cerebral artery markedly reduced infarct size, and this

90 enchyma, hydrocephalus, and so-called middle cerebral artery (MCA) "pseudofeeders" were correlated wi

91 The risk of seizures after malignant middle cerebral artery (MCA) infarction with decompressive hemi

92 The middle cerebral artery (MCA) is the second most common location

93 th acute ischemic stroke (AIS) due to middle cerebral artery (MCA) occlusion were enrolled; 75 underw

94 ted occlusive VWF-rich thrombi in the middle cerebral artery (MCA) of mice.

95 erior cerebral artery (ACA), and / or middle cerebral artery (MCA) secondary to SAH due to an aneurys

96 ients with internal carotid artery or middle cerebral artery (MCA) stroke and to evaluate the relatio

97 10), rats were sacrificed for either middle cerebral artery (MCA) structure and function assessments

98 GPIIb/IIIa antagonist tirofiban, in a middle cerebral artery (MCA) thrombosis model in guinea pigs.

99 Occlusion of the middle cerebral artery (MCA) with an endovascular filament is a

100 fined by location (at proximal/distal middle cerebral artery (MCA), within/beyond diffusion-weighted

101 l artery (VA) and CBF velocity at the middle cerebral artery (MCA).

102 following photochemical injury to the middle cerebral artery (MCA).

103 al transcranial Doppler (aTCD) on the middle cerebral artery (MCA): MCA pulsatility index (PIa) and a

104 in Eln(+/-) than Eln(+/+) mice in the middle cerebral artery (MCA, P < 0.001), but was similar betwee

105 nge, 5-17]), of the M1 segment of the middle cerebral artery (MCA; 52 patients: median NIHSS score, 1

106 Cerebral blood velocity in the middle cerebral artery (MCAv) was obtained by transcranial Dopp

107 ime-averaged mean of maximum velocities in 8 cerebral arteries, measured by TCD (TCD velocity) at 1 y

108 tion imaging, enabling surgeons to visualize cerebral arteries' microstructure and micron-level featu

109 d to have watershed infarcts in the anterior cerebral artery-middle cerebral artery and middle cerebr

110 Malignant middle cerebral artery [MMCA] infarction has a different topogr

111 e included 67 patients with malignant middle cerebral artery [MMCA] stroke who underwent decompressiv

112 angiotensin II stimulates TRPM4 currents in cerebral artery myocytes and vasoconstriction of cerebra

113 e BK (cbv1 + beta1) channels cloned from rat cerebral artery myocytes with a potency (EC(5)(0) = 53 m

114 and accessory beta1 subunits cloned from rat cerebral artery myocytes.

115 blotting detected LRRC26 mRNA and protein in cerebral artery myocytes.

116 eadaches and reversible segmental multifocal cerebral artery narrowing.

117 one augmentation in mesenteric and olfactory cerebral arteries; neither HFD nor STZ alone had an effe

118 hown to depolarize/constrict pressurized rat cerebral arteries; no effect was observed in CaV3.2(-/-)

119 In this study, a permanent middle cerebral artery occluded (MCAO) rat model was used.

120 sults CT scans from 100 patients with middle cerebral artery occlusion (44 women [mean age +/- standa

121 calculated in patients with proximal middle cerebral artery occlusion (derivation cohort) with known

122 , 5 and 7 days after permanent distal middle cerebral artery occlusion (dMCAO) in mice compared to ve

123 e rats received a 90-min right distal middle cerebral artery occlusion (dMCAo).

124 initiated at 48 h after mouse distal middle cerebral artery occlusion (dMCAO).

125 ld-type mice were subjected to 1 h of middle cerebral artery occlusion (MCAO) and 24-72 h of reperfus

126 nhibitor, in a rat model of transient middle cerebral artery occlusion (MCAO) and an in vitro model o

127 he animals were subjected to a 2-hour middle cerebral artery occlusion (MCAO) and sacrificed at 24 ho

128 odel encompasses a combination of the middle cerebral artery occlusion (MCAO) and spatial restraint s

129 to the ischemic site after transient middle cerebral artery occlusion (MCAO) followed by reperfusion

130 study, the model of reversible right middle cerebral artery occlusion (MCAO) for 2 h was used.

131 Following transient middle cerebral artery occlusion (MCAO) in adult rats, expressi

132 followed by continuous decline after middle cerebral artery occlusion (MCAO) in the mouse brain.

133 Ischemia induced either by embolic middle cerebral artery occlusion (MCAO) in vivo or by oxygen an

134 tion of Ang-(1-7) following transient middle cerebral artery occlusion (MCAO) increased the amount of

135 e intravenous (IV) injection in a rat middle cerebral artery occlusion (MCAO) model of ischemia/reper

136 AE) model of multiple sclerosis and a middle cerebral artery occlusion (MCAO) model of stroke, LSR wa

137 Using an in vivo middle cerebral artery occlusion (MCAO) model only the 57kDa fr

138 n injury in mouse photothrombotic and middle cerebral artery occlusion (MCAo) models.

139 UCHL1 C152A KI and WT mice underwent middle cerebral artery occlusion (MCAO) or sham surgery.

140 ale rats were subjected to a two-hour middle cerebral artery occlusion (MCAO) procedure.

141 1620-treated rats following permanent middle cerebral artery occlusion (MCAO) showed significant impr

142 Using the mouse middle cerebral artery occlusion (MCAO) stroke model, we have e

143 size of penumbra in mice subjected to middle cerebral artery occlusion (MCAO) using a genome-wide app

144 Infarct sizes 72 h after 60 min middle cerebral artery occlusion (MCAo) were on average 30 +/-

145 pite smaller infarcts after transient middle cerebral artery occlusion (MCAO) with the suture model.

146 In a mouse model of middle cerebral artery occlusion (MCAO), p38 MAPK activation wa

147 ia induced by permanent and transient middle cerebral artery occlusion (MCAO), we observed an initial

148 es) was induced by intraluminal right middle cerebral artery occlusion (MCAO).

149 erfusion after a 90-minute unilateral middle cerebral artery occlusion (MCAO).

150 Rats in the model groups underwent middle cerebral artery occlusion (MCAO).

151 a was induced by a transient (90 min) middle cerebral artery occlusion (MCAO).

152 ts with experimental stroke caused by middle cerebral artery occlusion (MCAO).

153 proteins, following a 1-h reversible middle cerebral artery occlusion (MCAO).

154 rological deficits after the onset of middle cerebral artery occlusion (MCAO).

155 55/262/279/282A) (MK4) on a permanent middle cerebral artery occlusion (pMCAO) stroke model.

156 infarction using a stroke model with middle cerebral artery occlusion (see figure).

157 mouse brains following 1 h transient middle cerebral artery occlusion (tMCAO) and measured real-time

158 trating myeloid cells after transient middle cerebral artery occlusion (tMCAO) in neonatal mice of bo

159 Furthermore, by transient middle cerebral artery occlusion (tMCAO) in rats, the transcrip

160 We induced transient middle cerebral artery occlusion (tMCAO) in T2D/obese mice (aft

161 A transient middle cerebral artery occlusion (tMCAO) model was used to esta

162 ronic diaschisis by using a transient middle cerebral artery occlusion (tMCAO) rat model.

163 rial thrombosis models: the transient middle cerebral artery occlusion (tMCAO) stroke model and tail

164 rct volumes 3 and 7 d after transient middle cerebral artery occlusion (tMCAo), independent of changi

165 corresponding controls, to transient middle cerebral artery occlusion (tMCAO).

166 ere subjected to 60 min of reversible middle cerebral artery occlusion and evaluated for infarct volu

167 Imaging revealed left middle cerebral artery occlusion and left transverse and sigmoi

168 Adipor gene expression in mice after middle cerebral artery occlusion and lipopolysaccharide injecti

169 e model of focal cerebral ischemia by middle cerebral artery occlusion and reperfusion (I/R) in male

170 In vivo, transient middle cerebral artery occlusion and reperfusion in kinase-dead

171 ts were subjected to right hemisphere middle-cerebral artery occlusion and reperfusion.

172 ns, while applying a remote transient middle cerebral artery occlusion as a model for ischemic stroke

173 ng the EcoHIV infection model and the middle cerebral artery occlusion as the ischemic stroke model i

174 patients who had ischaemic stroke and major cerebral artery occlusion beyond 3 h of symptom onset.

175 its and poststroke inflammation after middle cerebral artery occlusion by preventing microglia polari

176 e scores at those times, and proximal middle cerebral artery occlusion demonstrated prior to treatmen

177 either sex challenged with transient middle cerebral artery occlusion developed significantly smalle

178 volume of mice subjected to transient middle cerebral artery occlusion even up to 3 to 5 hours after

179 ate controls were subjected to 1 hour middle cerebral artery occlusion followed by 28-day reperfusion

180 Male Swiss Webster mice underwent middle cerebral artery occlusion for 1 h followed by reperfusio

181 Mice were subjected to middle cerebral artery occlusion for 40 min, followed by reperf

182 ebral ischemia was induced in mice by middle cerebral artery occlusion for 60 minutes and s-NSCs were

183 Sprague-Dawley rats were subjected to middle cerebral artery occlusion for 70 min followed by reperfu

184 ne the role of AhR in stroke, we used middle cerebral artery occlusion in mice and oxygen-glucose dep

185 the severity of stroke in a model of middle cerebral artery occlusion in mice.

186 spontaneous functional recovery after middle cerebral artery occlusion in mice.

187 y, and cerebral edema formation after middle cerebral artery occlusion in mice.

188 and until completion of 15 min distal middle cerebral artery occlusion in spontaneously hypertensive

189 in the ischemic brain after transient middle cerebral artery occlusion leading to increased intracran

190 We used a transient middle cerebral artery occlusion model to induce stroke and exa

191 cerebrovascular protection in a mouse middle cerebral artery occlusion model.

192 en used the murine suture and embolic middle cerebral artery occlusion models of stroke to investigat

193 oglial activation in infarcted distal middle cerebral artery occlusion mouse brain tissue more accura

194 y rats (12 months old) with permanent middle cerebral artery occlusion or sham operations on multiple

195 Methods: After distal middle cerebral artery occlusion or sham surgery, mice underwen

196 ensive rats and were subjected to 1-h middle cerebral artery occlusion or sham surgery.

197 TAT-C1aB in mice following transient middle cerebral artery occlusion significantly reduced ischemic

198 In the model of transient middle cerebral artery occlusion stroke Gna(i2)(fl/fl)/PF4-Cre

199 this study, using a murine transient middle cerebral artery occlusion stroke model, a novel therapeu

200 ment of blood flow anomaly in a mouse middle cerebral artery occlusion stroke model.

201 s implanted with CTX-DP 4 weeks after middle cerebral artery occlusion stroke prompted investigation

202 We investigated in a murine model of middle cerebral artery occlusion the effect of blocking SIDS by

203 Following middle cerebral artery occlusion to induce stroke in mice, immu

204 fecal transplant gavage 3 days after middle cerebral artery occlusion using young donor biome (2-3 m

205 ere reperfusion after photothrombolic middle cerebral artery occlusion was increased in Klkb1(-/-) mi

206 ollowing experimental stroke, using a middle cerebral artery occlusion with reperfusion model.

207 Middle cerebral artery occlusion with reperfusion was performed

208 rtery occlusion and 360 with isolated middle cerebral artery occlusion).

209 trophic lateral sclerosis (SOD1G93A), middle cerebral artery occlusion, and multiple mini-strokes.

210 Following transient middle cerebral artery occlusion, ck2beta(-/-) mice displayed s

211 rious microvascular settings, such as middle cerebral artery occlusion, femoral artery clipping, and

212 We found that after transient middle cerebral artery occlusion, inhibiting PlexinD1 signaling

213 hemic stroke and in mice subjected to middle cerebral artery occlusion, natural killer (NK) cells dis

214 thrombotic cortical injury, transient middle cerebral artery occlusion, or neonatal hypoxic-ischemic

215 In a mouse model of thrombin-induced middle cerebral artery occlusion, the efficacy of the diabody w

216 (BM) chimeras subjected to transient middle cerebral artery occlusion, we found that CD36(-/-) mice

217 ver, using a mouse model of transient middle cerebral artery occlusion, we observed that cerebral inf

218 Using two distinct models of acute middle cerebral artery occlusion, we show by next-generation se

219 ologically induced excitotoxicity and middle cerebral artery occlusion-induced brain damage.

220 l vascular endothelial cell death and middle cerebral artery occlusion-triggered cerebrovascular dama

221 nctional recovery following permanent middle cerebral artery occlusion.

222 ischemia was induced by 30 minutes of middle cerebral artery occlusion.

223 in the brains of 2D2 mice 14 d after middle cerebral artery occlusion.

224 tes AhR activation in the brain after middle cerebral artery occlusion.

225 ittermates received sham or transient middle cerebral artery occlusion.

226 were subjected to ischemic stroke by middle cerebral artery occlusion.

227 weeks into the treatment by transient middle cerebral artery occlusion.

228 80 male rats underwent 90-min middle cerebral artery occlusion.

229 ed ischemia by transient or permanent middle cerebral artery occlusion.

230 Cerebral ischemia was induced by middle cerebral artery occlusion.

231 85% reduction of infarct volume after middle cerebral artery occlusion; 54% rescue of low skeletal mu

232 ients with internal carotid artery or middle cerebral artery occlusions transferred over an 11-month

233 ternal carotid artery or the proximal middle cerebral artery occlusions we found that an infarct core

234 l carotid, basilar, and M1 segment of middle cerebral artery occlusions).

235 CA was induced in the right anterior cerebral artery-olfactory artery (ACA/OA) bifurcations i

236 of the internal carotid, basilar, and middle cerebral arteries on the first day at high altitude.

237 l artery sign is an appearance of the middle cerebral artery on non-contrast-enhanced computed tomogr

238 occlusion (internal carotid artery or middle cerebral artery) on outcomes.

239 l artery or a single supply by the posterior cerebral artery only.

240 n 2013 and 2014 for occlusions in the middle cerebral artery or carotid terminus by using a stent ret

241 rt study, we studied 72 patients with middle cerebral artery or terminal internal carotid artery occl

242 ity and the mean flow velocity in the middle cerebral artery (p = 0.0008).

243 g artery (Pcom), first part of the posterior cerebral artery (P1) and basilar artery was observed in

244 rtery, anterior communicating artery, middle cerebral artery, persistent stapedial artery and fenestr

245 ral artery-middle cerebral artery and middle cerebral artery-posterior cerebral artery watershed zone

246 ion and tortuous anatomic characteristics of cerebral arteries, present devices still risk failing to

247 We used a higher umbilical/cerebral artery pulsatility index ratio as an indicator

248 of KV1-C peptide to cannulated, pressurized cerebral arteries rapidly induced vasoconstriction and d

249 ed in smooth muscle cells of resistance-size cerebral arteries, resides primarily in the plasma membr

250 oxygen saturation (P = 0.007) and low middle cerebral artery resistive index (P = 0.04) were associat

251 ized the clot in the internal carotid/middle cerebral artery segment of all rats.

252 Coexistence of hyperdense middle cerebral artery sign and pulmonary thromboembolism is ve

253 emale patient who had both hyperdense middle cerebral artery sign and pulmonary thromboembolism.

254 Hyperdense middle cerebral artery sign is an appearance of the middle cere

255 ssures and systolic velocities of the middle cerebral artery significantly decreased (p < 0.01) after

256 iffness and increases in maximal diameter of cerebral arteries signify that elevations in brain blood

257 TRPP2 is the major TRPP isoform expressed in cerebral artery smooth muscle cells, with message levels

258 e primary sensor of intraluminal pressure in cerebral artery smooth muscle cells.

259 and approximately 45-fold higher in isolated cerebral artery smooth muscle cells.

260 is retrospective study, patients with middle cerebral artery stroke due to proximal occlusion from 20

261 ed ALD-401 in patients with disabling middle cerebral artery stroke in comparison with sham harvest w

262 on In this study, patients with acute middle cerebral artery stroke with absence of cortical vein opa

263 nt infarction in the territory of the middle cerebral artery, TAT.ARC salvages brain tissue when give

264 n had low or uninterpretable baseline middle cerebral artery TCD velocities, which were associated wi

265 white matter tracts, and involved the middle cerebral artery territory for 112 patients (73%).

266 mputed tomography (ie, over one-third middle cerebral artery territory hypodensity).

267 luded memory impairment and a left posterior cerebral artery territory infarction.

268 r asymmetries of blood flow in the posterior cerebral artery territory.

269 igher rate of recanalization of the affected cerebral artery than systemic intravenous thrombolytic t

270 nt of complete ligation and nerve density in cerebral arteries that were stained for the general neur

271 Conclusion In acute stroke of the middle cerebral artery, the Alberta Stroke Program Early CT sco

272 s generated by occlusion of the right middle cerebral artery, then 90 min later, stroke rats were ran

273 the relatively high-oxygen and high-velocity cerebral arteries to the relatively low-oxygen and low-v

274 ral artery was a ratio of flow in the middle cerebral artery to extracranial internal carotid artery

275 mice with thrombotic occlusion of the middle cerebral artery, tPA administration increased brain hemo

276 l CBFV recordings from left and right middle cerebral arteries using 20 healthy subjects (10 females)

277 Specific posterior cerebral artery variants were associated with greater as

278 ontralateral ratio of the activity in middle cerebral artery-vascularized territories in each hemisph

279 The prevalence of middle cerebral artery vasospasm in children with moderate trau

280 of CBF and extra-cranial blood flow), middle cerebral artery velocity (MCA Vmean), arterial-venous di

281 ation, blood pressure, heart rate and middle cerebral artery velocity (MCAv) were measured during the

282 ernal carotid artery vs M1 segment of middle cerebral artery vs M2 segment of middle cerebral artery)

283 Doppler ultrasound monitoring of the middle cerebral arteries was performed whenever possible to cla

284 Mean duration of vasospasm in the middle cerebral artery was 2 days (+/- 2 d) and 1.5 days (+/- 1

285 quired for vasospasm diagnosis in the middle cerebral artery was a ratio of flow in the middle cerebr

286 Median mean flow velocity in the middle cerebral artery was low (27.0 cm/s [23.8-30.5 cm/s]) at

287 Narrowing of A1 segment of anterior cerebral artery was noted in 9 patients (9.18%), of the

288 arrow (BM) chimeric mice in which the middle cerebral artery was occluded and infarct volume was dete

289 Middle cerebral artery was occluded for 12 to 60 minutes in mic

290 artery and middle cerebral artery-posterior cerebral artery watershed zones in addition to bilateral

291 3D reconstructions of cerebral arteries were created based on the data.

292 and lysosomes in freshly isolated SMCs from cerebral arteries were essentially immobile.

293 Rat cerebral arteries were used for analyses.

294 cal features of the segments of the anterior cerebral artery were acquired on a sample and intra-pati

295 ranial internal carotid, \basilar, or middle cerebral artery were included less than 4.5 hours after

296 ocytes of both rat and human resistance-size cerebral arteries, where it locates to both the nucleus

297 H disrupted dilatory NO signaling ex vivo in cerebral arteries, which shifted vascular tone balance f

298 l internal carotid artery or proximal middle cerebral artery who had last been known to be well 6 to

299 ibution of blood flow to posteriorly located cerebral arteries with remarkable changes in morphology

300 induced by temporary occlusion of the middle cerebral artery with a microfilament.