ライフサイエンスコーパス: cerebral artery

1 via endovascular perforation of the anterior cerebral artery.

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

3 Sprague Dawley rats by occluding the middle cerebral artery.

4 nt 90 min transient occlusions of the middle cerebral artery.

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

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

7 bral artery myocytes and vasoconstriction of cerebral arteries.

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

9 currents to induce myogenic constriction of cerebral arteries.

10 ron pathway may promote virus persistence in cerebral arteries.

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

12 voked constriction of pressurized rat middle cerebral arteries.

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

14 change in the mechanical properties of mouse cerebral arteries.

15 nching at bifurcations of the major proximal cerebral arteries.

16 asoconstriction and structural remodeling of cerebral arteries.

17 ng the hemodynamics characteristics of major cerebral arteries.

18 tion of abnormalities and normal variants of cerebral arteries.

19 ions in smooth muscle cells of rat and human cerebral arteries.

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

21 functional significance in myocytes of small cerebral arteries.

22 e primary sensor of intraluminal pressure in cerebral arteries.

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

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

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

26 sions were frequently detected in the middle cerebral artery (23%), internal carotid artery (13%), an

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

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

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 With CE-muMRA, cerebral arteries and veins with a diameter of less than

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

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

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

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

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

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

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

43 near-infrared spectroscopy along with middle cerebral artery blood flow measured using transcranial D

44 In the middle cerebral artery blood flow velocities and vasomotor reac

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

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

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

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

49 Patients with significant carotid or middle-cerebral artery disease or impaired vasoreactivity were

50 Coordinately, isolated posterior cerebral arteries display augmented myogenic tone, which

51 ed by transient (1h) occlusion of the middle cerebral artery, during which mean arterial blood pressu

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

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

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

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

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

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

58 Mean cerebral artery flow velocity and jugular vein oxygen sa

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

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

61 Isolated cerebral arteries from HA fetuses showed a higher contra

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

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

64 he raw recordings from left and right middle cerebral arteries had higher content of mutual informati

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

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

67 atively low mean flow velocity in the middle cerebral artery in combination with normal jugular bulb

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

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

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

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

72 aps obtained less than 12 hours after middle cerebral artery infarct.

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

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

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

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

77 Survival after malignant middle cerebral artery infarcts is dismal.

78 Consecutive patients with M1 segment middle cerebral artery +/- intracranial internal carotid artery

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 The anterior cerebral artery is a common location of intracranial ane

82 In cerebral arteries, K(Ca)2.3 loss is associated with NO s

83 Deposition of amyloid-beta (Abeta) in cerebral arteries, known as cerebral amyloid angiopathy

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

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

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

87 rpolarization was investigated in rat middle cerebral arteries (MCA).

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

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

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

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

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

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

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

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

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

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

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

99 id artery (ICA), basilar artery (BA), middle cerebral artery (MCA)], the submandibular gland (SMG), a

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

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

102 m Hg vs. 41 +/- 2 mm Hg; p < .05) and middle cerebral artery mean flow velocity (37 +/- 9 cm.sec(-1)

103 and higher mean arterial pressure-to-middle cerebral artery mean flow velocity phase difference (p <

104 endotoxemia was associated with lower middle cerebral artery mean flow velocity variability (1.0 +/-

105 Systemic hemodynamics, middle cerebral artery mean flow velocity, and dynamic cerebral

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

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

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

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

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

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

112 ion was replicated on native channels in rat cerebral artery myocytes.

113 eadaches and reversible segmental multifocal cerebral artery narrowing.

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

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

116 useful in infarct volume reduction in middle cerebral artery occluded rat brain.

117 Vehicle-treated middle cerebral artery occluded rats demonstrated high levels o

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

119 , 5 and 7 days after permanent distal middle cerebral artery occlusion (dMCAO) in mice compared to ve

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

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

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

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

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

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

126 l of permanent and transient (45 min) middle cerebral artery occlusion (MCAO) during the hyperacute,

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

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

129 t male C57BL/6 mice were subjected to middle cerebral artery occlusion (MCAO) for stroke induction.

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

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

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

133 prove sensorimotor functions in a rat middle cerebral artery occlusion (MCAO) model after a single in

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

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

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

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

138 hemia was induced by permanent distal middle cerebral artery occlusion (MCAO) on day 14 of vehicle or

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

140 ague-Dawley rats undergoing permanent middle cerebral artery occlusion (MCAO) received three intraven

141 tudy, rats were sacrificed 24 h after middle cerebral artery occlusion (MCAO) stroke and gene transcr

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

143 GRN(+/-) and PGRN(-/-) mice underwent middle cerebral artery occlusion (MCAO) with monitoring of cere

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

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

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

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

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

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

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

151 T) mice were subjected to a transient middle cerebral artery occlusion (MCAO).

152 ittermate were subjected to 45 min of middle cerebral artery occlusion (MCAO).

153 ed to permanent, 60-min and 30-min of middle cerebral artery occlusion (MCAO).

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

155 129/SV mice were subjected to 30-min middle cerebral artery occlusion (MCAo)/reperfusion and serial

156 xcitatory neurotoxicity in reversible middle cerebral artery occlusion (rMCAO) model in vivo.

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

158 r evaluated in vivo using a transient middle cerebral artery occlusion (t-MCAO) model of stroke.

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

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

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

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

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

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

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

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

167 icient Rag1(-/-) mice after 60 min of middle cerebral artery occlusion and reperfusion.

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

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

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

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

172 of either sex subjected to transient middle cerebral artery occlusion developed dramatically smaller

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

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

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

176 We performed right middle cerebral artery occlusion for 3 hours, administered reco

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

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

179 othelin receptors following permanent middle cerebral artery occlusion for 7 days.

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

181 Animals were subjected to transient middle cerebral artery occlusion for 90 mins.

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

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

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

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

186 mbra when administered six hours post middle cerebral artery occlusion in rats.

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

188 erebral ischemia induced by transient middle cerebral artery occlusion it selectively dilates arterio

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

190 In the middle cerebral artery occlusion model, the volume and fraction

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

192 e C57BL/6 mice using the intraluminal middle cerebral artery occlusion model.

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

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

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

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

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

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

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

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

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

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

203 ed in mice (by permanent or transient middle cerebral artery occlusion) and rats (by 3-vessel occlusi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

218 ittermates received sham or transient middle cerebral artery occlusion.

219 Cerebral ischemia was induced by middle cerebral artery occlusion.

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

221 bra using a mouse model of reversible middle cerebral artery occlusion.

222 r bundles from degeneration following middle cerebral artery occlusion.

223 brains 6 h or 7 days after transient middle cerebral artery occlusion.

224 neonatal and adult rats by transient middle cerebral artery occlusion.

225 t cavity for 7 d, beginning 7 d after middle cerebral artery occlusion.

226 d into rat brains 6 h after transient middle cerebral artery occlusion.

227 85% reduction of infarct volume after middle cerebral artery occlusion; 54% rescue of low skeletal mu

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

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

230 tant with a mean flow velocity in the middle cerebral artery of 71.5 (56.0-78.5) at 108 hrs (p=.381).

231 Under anaesthesia, the middle cerebral artery of adult rats was occluded for 60 min us

232 - and medium-sized vessels, but not in large cerebral arteries, of 24-month-old arcAbeta mice.

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

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

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

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

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

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

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

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

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

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

243 ferences in mean flow velocity in the middle cerebral artery, pulsatility index, and jugular bulb oxy

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

245 arming, the mean flow velocity in the middle cerebral artery remained relatively constant with a mean

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

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

248 rly infarct signs (yes = 1) and (hyper)Dense cerebral artery sign (yes = 1) on admission computed tom

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

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

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

252 to 36 hours of a baseline hyperdense middle cerebral artery sign was increased (63% [124 of 196] vs

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

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

255 a expression is increased in mouse posterior cerebral artery smooth muscle cells at 6 weeks after myo

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

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

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

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

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

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

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

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

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

265 Three weeks after right middle cerebral artery territory injury, rats treated with 0.72

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

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

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

269 As compared with aneurysms in the middle cerebral arteries, those in the posterior and anterior c

270 of the GPIb-VWF axis in guinea pigs prevents cerebral artery thrombosis and induces early reperfusion

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

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

273 TNFalpha)-dependent enhancement of posterior cerebral artery tone that reduces cerebral blood flow be

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

275 nt difference in intracranial pressure, mean cerebral artery transcranial Doppler velocity, PaCO2, ce

276 -like extensions from arterioles of existing cerebral artery trees.

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

278 Specific posterior cerebral artery variants were associated with greater as

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

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

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

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

283 enous steroid lithocholic acid (LCA) dilates cerebral arteries via BK channel activation, which requi

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

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

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

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

288 Mean flow velocity in the middle cerebral artery was low (26.5 (18.7-48.0) cm/sec) at adm

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

290 Mean flow velocity in the middle cerebral artery was measured by transcranial Doppler at

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

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

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

294 Cerebral emboli entering the middle cerebral arteries were counted at baseline and every 6 m

295 3D reconstructions of cerebral arteries were created based on the data.

296 d examination of the extra- and intracranial cerebral arteries were enrolled consecutively.

297 Rat cerebral arteries were used for analyses.

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

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

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