ライフサイエンスコーパス: MCAO

1 MCAO also induced significant changes in forelimb use in

2 MCAO induced significant decline in neurological score p

3 MCAO markedly downregulated fibroblast growth factor-21

4 MCAO resulted in a substantial lesion formation and a si

5 MCAO resulted in ~60% larger infarcts in PGRN(+/-) and P

6 MCAO was induced for 30, 40 or 60 min in ovariectomized

7 MCAO was performed 48 h after the last dose of E-selecti

8 MCAO-induced lesion volumes were greater in insulinopeni

9 mly assigned to Sham-operated mice (n = 10), MCAO mice receiving the vehicle (n = 15) and MCAO mice r

10 cular method for this was published in 1989, MCAO has been applied commonly to the rat, and often pai

11 ry occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for comparison.

12 After MCAO, mitochondrial dysfunction was augmented more signi

13 al deficit scores were quantitated 24h after MCAO.

14 he ischemic hemisphere on Days 1 and 3 after MCAO, and were significantly restored by TubA.

15 administered thrice: 30 min, 2h and 4h after MCAO for a total dose of 3 mg/kg) on cerebral ischemia i

16 loss and similar astrocyte activation after MCAO than their wild-type littermates.

17 were sequentially acquired before and after MCAO/R.

18 did not diminish the increase in CNTF after MCAO.

19 O followed by reperfusion and then 1 d after MCAO received an intravenous injection of either PBS (co

20 ree of total tissue loss measured 90 d after MCAO was quite modest.

21 were evaluated by SPECT/CT up to 14 d after MCAO.

22 active astrocytic response is dampened after MCAO.

23 y for 2 to 4 weeks from the fourth day after MCAO induced PSD-like depressive phenotypes in mice.

24 iately after surgery, 3, 7 and 10 days after MCAO).

25 ial effects lasted at least three days after MCAO.

26 enuated cortical lesion size at 7 days after MCAO.

27 logical stress but will be exacerbated after MCAO.

28 Infarct size was measured at 22 h after MCAO in estradiol-treated OVX animals in the presence an

29 d ischemic infarct size at 24 and 72 h after MCAO surgery.

30 hemic cortex cytosolic fraction at 3 h after MCAO without affecting T-STAT3.

31 At 3 h after MCAO, ADC and CBF lesions showed similar robust correlat

32 er activity rates at both 2 h and 24 h after MCAO, associated with significant fewer apoptotic cells

33 ificantly reduced infarct size at 24 h after MCAO.

34 ction, which remained elevated at 22 h after MCAO.

35 volume defined by TTC staining at 24 h after MCAO.

36 functional neurological deficits 48 h after MCAO.

37 volumes (mm(3)) calculated At 24 hours after MCAO, and infarct volume was determined using triphenylt

38 Twenty-four hours after MCAO, apoptosis was further increased in both diabetic m

39 Notably, when given at 24 hours after MCAO, TubA still exhibited significant protection.

40 isolated cerebral microvessels in mice after MCAO.

41 dosage of 2.5 U/kg body weight 30 min after MCAO (MCAO duration=60 min) and again 24 h after reperfu

42 flow maps through the first 60 minutes after MCAO; but not after 90 minutes of occlusion.

43 eases STAT3 phosphorylation in neurons after MCAO and that STAT3 activation plays an important role i

44 ypothesized that HBO given prior to or after MCAO reduces PMN infiltration into the brain, and that d

45 nclusion, our results demonstrate that after MCAO the interaction between tPA and LRP results in NF-k

46 ice received treatment with murine tPA after MCAO.

47 Mortality at 1 week after MCAO/R in the acutobin-treated group was significantly l

48 eatment, and mice were killed 12 weeks after MCAO.

49 the ability of estradiol to protect against MCAO-induced cell death involves attenuation of c-Fos in

50 MCAO mice receiving the vehicle (n = 15) and MCAO mice receiving an anti-myostatin PINTA745 (n = 12;

51 hondrial cyt c release at 24 h post-CCI and -MCAO.

52 ary occlusion of the middle cerebral artery (MCAO) to produce ischemia.

53 lic occlusion of the middle cerebral artery (MCAO).

54 rom ischemic insult when administered before MCAO, probably by limiting damage mediated by detrimenta

55 a-estradiol (E2) or vehicle (OVX) 2 h before MCAO and sacrificed 24 h after the indicated duration of

56 Administration of LPS 24 h before MCAO reduced the infarct by 68% and improved ischemic ce

57 e was injected intraperitoneally 24 h before MCAO.

58 ated mice from nasally tolerized mice before MCAO surgery decreased stroke size (p < 0.001 vs control

59 nd 30 mg/kg, i.p. administered 15 min before MCAO) produced 43% (n = 8, p = 0.16) and 58% (n = 8, p <

60 mg/kg (n=6), or 3 mg/kg (n=7) 30 min before MCAO.

61 es in GLAST or EAAC1 mRNA expression between MCAO and sham-operated brains.

62 od/brain barrier function was compromised by MCAO in WT mice.

63 ic responses and brain infarction induced by MCAO and reperfusion.

64 ear factor (NF)-kappaB activation induced by MCAO were unaffected by lack of CD36.

65 ion in cerebrovascular regulation induced by MCAO, as demonstrated by normalization of the increase i

66 To characterize metabolic changes induced by MCAO, we have induced permanent MCAO in mice that were i

67 CD14, a co-receptor of TLR4, was induced by MCAO, while the expression of TLR4 remained unchanged.

68 these brain areas were assessed by comparing MCAO brains with sham-operated control brains.

69 In contrast, MCAO-induced microglial activation is significantly decr

70 Second, we tested in a distal MCAO model.

71 lantation was performed 14 days after distal MCAO and doublecortin (Dcx)-expressing cells in the subv

72 n-weighted magnetic resonance imaging during MCAO was similar in neonatal CD36ko and WT mice, by 24 h

73 ller in GK rats with both suture and embolic MCAO, but expanded with longer reperfusion period.

74 ith the suture model, but not in the embolic MCAO.

75 irst, we tested gemfibrozil in a filamentous MCAO model.

76 Finally, MCAO: infarct volumes were not statistically different a

77 Following MCAO, mice were treated IV with low (1000 U/kg) and high

78 s of the hippocampus were analyzed following MCAO.

79 sis of Ets-1 protein in rat brains following MCAO showed that Ets-1 was highly expressed in neurons i

80 change in cerebral ischemic damage following MCAO in rats.

81 degeneration from 10 min to 7 days following MCAO was established.

82 The neurological deficit following MCAO was lower and oxidative stress parameters were impr

83 d to prevent cortical degeneration following MCAO in SIRT5-/- mice.

84 eral Aquaporin-4 (AQP4) expression following MCAO or progesterone treatment.

85 At 24 h following MCAO, blood-brain barrier permeability (BBB), stroke inf

86 se in the contralateral hemisphere following MCAO and diminished antioxidant capacity in the brain as

87 O dramatically reduced infarctions following MCAO.

88 the volume of the ischemic lesion following MCAO in wild-type and tPA-deficient (tPA-/-) neurons and

89 the volume of the ischemic lesion following MCAO.

90 ed rats had significant protection following MCAO induced cerebral ischemia.

91 reptozotocin-induced diabetic rats following MCAO with reperfusion.

92 r therapeutic intervention in rats following MCAO.

93 ain injury and functional recovery following MCAO and tPA reperfusion was assessed in young adult and

94 By 1 week following MCAO, VEGF-positive vessels/30 microm brain slice in the

95 ateral hemisphere volumes were 34 +/- 7% for MCAO, 24 +/- 6% for isoflurane preconditioning plus MCAO

96 Furthermore, MCAO caused nuclear translocation of the intracellular d

97 Rats underwent a 1-h MCAO followed by reperfusion and then 1 d after MCAO rec

98 Reperfusion after a 2 h MCAO compared to 24 h MCAO was associated with a decreas

99 esion volume and apoptosis subsequent to 2-h MCAO followed by 24-h reperfusion.

100 apoptotic levels in animals subjected to 2-h MCAO followed by 24-h reperfusion.

101 eperfusion after a 2 h MCAO compared to 24 h MCAO was associated with a decrease in TUNEL staining an

102 and CD40L-deficient mice subjected to 1-hour MCAO and 4-hour reperfusion.

103 oflurane anesthesia) and subjected to 2-hour MCAO.

104 In MCAO in adult rats, H(2) gas therapy demonstrated a tren

105 treated group which were severely altered in MCAO group.

106 ring a muscle contraction were attenuated in MCAO rats when compared to sham rats.

107 contraction were significantly attenuated in MCAO rats when compared to sham rats.

108 esponses during static muscle contraction in MCAO rats is partly due to a reduction in nNOS expressio

109 cular responses during muscle contraction in MCAO rats may be partly due to a reduction in eNOS expre

110 tion, and ameliorated neuronal cell death in MCAO rats.

111 of tPA resulted in a significant decrease in MCAO-induced nitric oxide production and inducible nitri

112 s 1, 3, 5, 7 post-ischemia, respectively) in MCAO subjected rats.

113 e subgrouped based on amount of tissue loss, MCAO animals with only 4% tissue loss exhibited enduring

114 e of 2.5 U/kg body weight 30 min after MCAO (MCAO duration=60 min) and again 24 h after reperfusion.

115 In the 30-min MCAO group, multiple time-point analysis showed no stati

116 o implants 7 days prior to undergoing 60 min MCAO.

117 In the 60-min MCAO group, multiple time-point analysis improved specif

118 We found that a 60-minute MCAO followed by spatial restraint stress for 2 h daily

119 were serially obtained in rat stroke models (MCAO): permanent, 90 min, and 180 min temporary MCAO.

120 of cl-nanozyme in a well-characterized mouse MCAO model of I/R injury.

121 nt right middle cerebral arterial occlusion (MCAO) in adult male rats.

122 to 1 h of middle cerebral artery occlusion (MCAO) and 24-72 h of reperfusion.

123 transient middle cerebral artery occlusion (MCAO) and an in vitro model of excitotoxicity.

124 esponse to middle cerebral artery occlusion (MCAO) and reperfusion.

125 transient middle cerebral artery occlusion (MCAO) and reperfusion.

126 o a 2-hour middle cerebral artery occlusion (MCAO) and sacrificed at 24 hours of reperfusion.

127 ion of the middle cerebral artery occlusion (MCAO) and spatial restraint stress.

128 caused by middle cerebral artery occlusion (MCAO) and traumatic brain injury (TBI) caused by control

129 transient middle cerebral artery occlusion (MCAO) as was estrone.

130 t (45 min) middle cerebral artery occlusion (MCAO) during the hyperacute, acute and chronic phases.

131 transient middle cerebral artery occlusion (MCAO) followed by reperfusion in rats and potentiate the

132 reversible middle cerebral artery occlusion (MCAO) for 1 hour followed by 1 hour of reperfusion.

133 d to right middle cerebral artery occlusion (MCAO) for 2 h under ketamine/xylazine or isoflurane anes

134 ible right middle cerebral artery occlusion (MCAO) for 2 h was used.

135 bjected to middle cerebral artery occlusion (MCAO) for stroke induction.

136 permanent middle cerebral artery occlusion (MCAO) group, respectively.

137 ed H(2) in middle cerebral artery occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for compari

138 transient middle cerebral artery occlusion (MCAO) in adult rats, expression of FosDT and Fos was ind

139 24h after Middle Cerebral Artery Occlusion (MCAO) in all 3 types of mice.

140 90 min of middle cerebral artery occlusion (MCAO) in male Wistar rats.

141 rated that middle cerebral artery occlusion (MCAO) in mice induces shedding of the LRP ectodomain, we

142 following middle cerebral artery occlusion (MCAO) in ovariectomised female mice, with a physiologica

143 ecovery to middle cerebral artery occlusion (MCAO) in rats and hMCT2 transgenic mice and of hippocamp

144 size after middle cerebral artery occlusion (MCAO) in rats through an unknown mechanism.

145 ter distal middle cerebral artery occlusion (MCAO) in rats.

146 permanent middle cerebral artery occlusion (MCAO) in SHR-SP rats and whether these effects are relat

147 30 min of middle cerebral artery occlusion (MCAO) in the mouse brain in both the ischemic core and p

148 line after middle cerebral artery occlusion (MCAO) in the mouse brain.

149 by embolic middle cerebral artery occlusion (MCAO) in vivo or by oxygen and glucose deprivation in br

150 perimental middle cerebral artery occlusion (MCAO) increases tPA activity and neuroserpin expression

151 found that middle cerebral artery occlusion (MCAO) induces microglial activation in both wild-type an

152 Middle cerebral artery occlusion (MCAO) is a popular model in experimental stroke research

153 traluminal middle cerebral artery occlusion (MCAO) method.

154 s in a rat middle cerebral artery occlusion (MCAO) model after a single intravenous (i.v.) injection.

155 sion in a permanent middle artery occlusion (MCAO) model in rats.

156 permanent middle cerebral artery occlusion (MCAO) model in the adult mouse.

157 nsient rat middle cerebral artery occlusion (MCAO) model of brain ischemia.

158 permanent middle cerebral artery occlusion (MCAO) model of focal ischemia.

159 n in a rat middle cerebral artery occlusion (MCAO) model of ischemia/reperfusion (I/R) injury (stroke

160 osis and a middle cerebral artery occlusion (MCAO) model of stroke, LSR was down-regulated, linking l

161 an in vivo middle cerebral artery occlusion (MCAO) model only the 57kDa fragment of MetAP2 was observ

162 dovascular middle cerebral artery occlusion (MCAO) model to examine the influence of NF-kappaB on neu

163 the mouse middle cerebral artery occlusion (MCAO) model.

164 permanent middle cerebral artery occlusion (MCAO) models in young adult male mice on normal diet.

165 ent distal middle cerebral artery occlusion (MCAO) on day 14 of vehicle or GCV treatment, and mice we

166 nar suture middle cerebral artery occlusion (MCAO) procedure was used to produce small infarcts in mi

167 a two-hour middle cerebral artery occlusion (MCAO) procedure.

168 ive in the middle cerebral artery occlusion (MCAO) rat stroke model.

169 permanent middle cerebral artery occlusion (MCAO) received three intravenous injections of either ve

170 transient middle cerebral artery occlusion (MCAO) reduced infarct volume by >50%; the protection per

171 24 h after middle cerebral artery occlusion (MCAO) stroke and gene transcription in brain tissues fol

172 mice after middle cerebral artery occlusion (MCAO) strongly implicates a mixture of both pathogenic a

173 e model of middle cerebral artery occlusion (MCAO) to examine whether improvements in cerebrovascular

174 ice before middle cerebral artery occlusion (MCAO) to induce an anti-inflammatory T cell response dir

175 t model of middle cerebral artery occlusion (MCAO) under two anesthesia regimens.

176 permanent middle cerebral artery occlusion (MCAO) was induced by intraluminal filament.

177 following middle cerebral artery occlusion (MCAO) when compared to non-diabetics.

178 underwent middle cerebral artery occlusion (MCAO) with monitoring of cerebral blood flow.

179 following middle cerebral artery occlusion (MCAO) with or without reperfusion.

180 transient middle cerebral artery occlusion (MCAO) with the suture model.

181 y utilized middle cerebral artery occlusion (MCAO) with tissue plasminogen activator (tPA) to assess

182 to 2 h of middle cerebral artery occlusion (MCAO), and phosphorylated STAT3 (P-STAT3) and total STAT

183 received a middle cerebral artery occlusion (MCAO), and T(2)-weighted MRI at 48 h post-MCAO quantifie

184 traluminal middle cerebral artery occlusion (MCAO), or SHAM surgery.

185 e model of middle cerebral artery occlusion (MCAO), p38 MAPK activation was observed in the glia scar

186 s with the middle cerebral artery occlusion (MCAO), provided the BDNF is conjugated to a blood-brain

187 transient middle cerebral artery occlusion (MCAO), we observed an initial elevation ( 1.7-fold, 1-4

188 ts against middle cerebral artery occlusion (MCAO)-induced brain injury during late phases of neurona

189 ex against middle cerebral artery occlusion (MCAO)-induced cell death.

190 P plays on middle cerebral artery occlusion (MCAO)-induced NF-kappaB-mediated inflammatory response.

191 48h after middle cerebral artery occlusion (MCAO).

192 permanent middle-cerebral artery occlusion (MCAO).

193 transient middle cerebral artery occlusion (MCAO).

194 bjected to middle cerebral artery occlusion (MCAO).

195 transient middle cerebral artery occlusion (MCAO).

196 t model of middle cerebral artery occlusion (MCAO).

197 following middle cerebral artery occlusion (MCAO).

198 90 min of middle cerebral artery occlusion (MCAO).

199 temporary middle cerebral artery occlusion (MCAO).

200 underwent middle cerebral artery occlusion (MCAO).

201 t (90 min) middle cerebral artery occlusion (MCAO).

202 caused by middle cerebral artery occlusion (MCAO).

203 reversible middle cerebral artery occlusion (MCAO).

204 transient middle cerebral artery occlusion (MCAO).

205 45 min of middle cerebral artery occlusion (MCAO).

206 inal right middle cerebral artery occlusion (MCAO).

207 30-min of middle cerebral artery occlusion (MCAO).

208 transient middle cerebral artery occlusion (MCAO).

209 permanent middle cerebral artery occlusion (MCAO).

210 induced by middle cerebral artery occlusion (MCAO).

211 utilizes a mouse middle cerebral occlusion (MCAO) model of embolic stroke to study neuronal degenera

212 ttenuated following transient MCA occlusion (MCAO) and reperfusion, mediated via alteration of the ne

213 transient middle cerebral artery occlusions (MCAO) were induced for various duration, and protective

214 ontribution of B cells to the development of MCAO by comparing infarct volumes and functional outcome

215 rificed 24 h after the indicated duration of MCAO.

216 We examined the effects of MCAO on the temporospatial pattern of IEG expression and

217 ce were used to examine the exact effects of MCAO using Fluoro-Jade, a marker of neurodegeneration th

218 kg M40401 at 60 min of MCAO or at the end of MCAO (90 min) failed to significantly reduce lesion volu

219 nd phospho-ERK 1/2 expression after 1-2 h of MCAO (p<0.05).

220 ation at various survival times after 1 h of MCAO.

221 on rather than normal cerebral hemisphere of MCAO rats.

222 trophils in the affected brain hemisphere of MCAO-treated muMT(-/-) versus WT mice.

223 a single dose of 3 mg/kg M40401 at 60 min of MCAO or at the end of MCAO (90 min) failed to significan

224 area at 30 and 40 min, but not at 60 min of MCAO.

225 ter the initial drop in rCBF at the onset of MCAO.

226 to sham rats and the right CVLM quadrant of MCAO rats, eNOS expression was significantly increased i

227 to sham rats and the right CVLM quadrant of MCAO rats, nNOS expression was significantly augmented i

228 pha expression in the ipsilateral regions of MCAO-subjected rats was reduced after MMP-12 knockdown i

229 e ability of in vivo anti-ischemic stroke of MCAO rats.

230 tective potential of NRG-1 using a permanent MCAO ischemia (pMCAO) rat model.

231 After permanent MCAO, larger and more consistent infarct volumes resulte

232 ection was also demonstrated after permanent MCAO.

233 iol increased infarct volume after permanent MCAO.

234 Following permanent MCAO, infarct size was smaller, edema was greater, and t

235 s induced by MCAO, we have induced permanent MCAO in mice that were implanted with a microdialysis pr

236 In a mouse model of permanent MCAO, no significant difference in motor function recove

237 In the permanent MCAO group, prediction with multiple time-point diffusio

238 In the permanent MCAO group, the lesion volume on the ADC maps was signif

239 recovery of skeletal muscle mass in PINTA745-MCAO mice involved an increased expression of genes enco

240 P < 0.05 for isoflurane preconditioning plus MCAO to compare with MCAO alone or with SB203580 plus is

241 B203580 plus isoflurane preconditioning plus MCAO) and mimicked by an activator of these kinases, ani

242 4 +/- 6% for isoflurane preconditioning plus MCAO, and 30 +/- 6% for SB203580 plus isoflurane precond

243 B203580 plus isoflurane preconditioning plus MCAO, n = 8, P < 0.05 for isoflurane preconditioning plu

244 ssion significantly increased at 1 week post MCAO in the infarcted hemisphere of IRL-1620 treated rat

245 ) and neurological score at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome

246 On day 7 post-MCAO, neurological deficit-matched rats were assigned to

247 nctional recovery was tested for 7 days post-MCAO and brains processed for histological verification

248 hemia and this increase peaks at 7 days post-MCAO.

249 d during the test period in both groups post-MCAO.

250 ency was 30+/-7 s and 103+/-9 s at 24 h post-MCAO in the animals treated with BDNF alone and the BDNF

251 n (MCAO), and T(2)-weighted MRI at 48 h post-MCAO quantified ischemic damage.

252 score performance (from 22 to 11 at 2 h post-MCAO) in the vehicle-treated animals, which was not sign

253 At 2 and 24 h post-MCAO, neurological deficits were assessed.

254 d injected intravenously (i.v.) 6 hours post-MCAO with either 1 mg/kg PNU-120596 (treated group) or v

255 behavioral tests were performed 24 hrs post-MCAO.

256 In conclusion, testosterone replacement post-MCAO accelerated functional recovery in castrate rats, s

257 double labeled for SHP-1 at early times post-MCAO.

258 me) to 14 days (minimum infarct volume) post-MCAO.

259 After 4 weeks post-MCAO, the average infarct volume was not significantly d

260 latency was >200 s at 16 RPM in all rats pre-MCAO.

261 olume and mortality in the hyperglycemic rat MCAO/R model.

262 +/-50 to 117+/-55 mm(3) in the temporary rat MCAO model (90 min), and from 216+/-58 to 127+/-57 mm(3)

263 ebral artery occlusion (MCAO) in adult rats (MCAO n=9, MCAO+H(2)n=7) for comparison.

264 esis that the ability of estradiol to reduce MCAO-induced cell death involves attenuation of expressi

265 iddle cerebral artery occlusion/reperfusion (MCAO/R) model.

266 d in rats with a temporary 90-min left-sided MCAO followed by 24 h reperfusion (n = 10).

267 left ipsilateral CVLM quadrant in left-sided MCAO rats.

268 mented in the ipsilateral CVLM in left-sided MCAO rats.

269 Left-sided MCAO significantly decreased the expression of eNOS in t

270 in rats with a temporary 90-minute one-sided MCAO followed by 24 hour reperfusion.

271 Similarly, MCAO-induced infarcts were significantly greater in IH-e

272 ransient middle cerebral artery occlusion (t-MCAO) model of stroke.

273 n vivo, using two-photon microscopy in the t-MCAO stroke model.

274 Infarct volume after temporary MCAO with a CCA clip was significantly larger and variab

275 After temporary MCAO, the SAH rate was 12.5% with a 5-0 curved suture an

276 O): permanent, 90 min, and 180 min temporary MCAO.

277 We found that MCAO increased LRP expression primarily in astrocytes an

278 We found that MCAO induces an increase in gamma-secretase activity in

279 core at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome compared with sham-o

280 The MCAO procedure resulted in a significant infarct in the

281 s undergoing MCAO alone at 14 days after the MCAO.

282 both acute and chronic insulin decreased the MCAO-induced lesion volume and apoptosis.

283 t show any significant changes following the MCAO.

284 een, liver) 3 days after IV injection in the MCAO rat.

285 ively few laboratories have investigated the MCAO method in the mouse.

286 These MCAO-induced changes were completely prevented in B-cell

287 ed after systemic administration of BMSCs to MCAO rats is likely due to the cellular changes in blood

288 by different scoring methods as compared to MCAO group.

289 or sensorimotor function in rats exposed to MCAO.

290 nhibitor; 5 mg/kg) or saline 30 min prior to MCAO.

291 ncreased apoptosis in the CNS in response to MCAO, and restoration of blood flow especially in the in

292 as also observed in SHR-SP rats subjected to MCAO after adoptive transfer of splenocytes from E-selec

293 Transient MCAO in rats may therefore provide a pre-clinical model

294 ane-preconditioned rats than rats undergoing MCAO alone at 14 days after the MCAO.

295 One week later, rats underwent MCAO and brains were collected 1, 4, 8, 16, and 24 hr la

296 Forty rats underwent MCAO and were randomized to pretreatment with HBO (3 ATA

297 One week later, rats underwent MCAO, and brains were collected at 1, 4, 8, 16, and 24 h

298 after MMP-12 knockdown compared to untreated MCAO subjected rats.

299 istar and GK rats were subjected to variable MCAO by suture or embolus occlusion.

300 ne preconditioning plus MCAO to compare with MCAO alone or with SB203580 plus isoflurane precondition