ライフサイエンスコーパス: hind limb

1 virtually a complete absence of axons in the hind limb.

2 during development of angiogenesis in mouse hind limb.

3 onstriction in the collateral circuit of the hind limb.

4 n of programmed cell death in the developing hind limb.

5 completely interrupts lymphatic flow of the hind limb.

6 from a flaccid tail to complete paralysis of hind limbs.

7 e pathology of control injured contralateral hind limbs.

8 persisted for 14 days in ECFC + MPC-injected hind limbs.

9 of myelosuppressed bone marrow and ischemic hind limbs.

10 and porpoises) are unusual in the absence of hind limbs.

11 ighly induced in the vasculature of ischemic hind limbs.

12 the marrow and revascularization of ischemic hind limbs.

13 nable to knuckle walk; 4, no movement, drags hind limbs.

14 h naive Wistar Furth (WF) hosts received ACI hind limbs.

15 ed rejection-free survival of donor-specific hind limbs.

16 FSS-induced collateral vessel growth in rat hind limbs.

17 for nitrite-mediated reperfusion of ischemic hind limbs.

18 e showed better ability to stand up on their hind limbs: a typical exploratory behavior seen in healt

19 Lymphedema was induced in the right hind limb after a single fraction of 20 Gy radiation, po

20 s demonstrate improved perfusion in ischemic hind limb after mobilization of bone marrow progenitor c

21 cipients (LEW, RT1(1)) received vascularized hind-limb allografts from hybrid Lewis x Brown-Norway (F

22 erance induction in fully MHC-mismatched rat hind-limb allografts.

23 study eliminates this delay period in a rat hind limb allotransplantation model by performing mixed

24 The authors performed 30 hind-limb allotransplantations across the MHC barrier be

25 EGFR2-mediated) angiogenic signaling in both hind limb and bone marrow.

26 Most of the up-regulated genes in hind limb and brain are the same.

27 sion profiles have been studied in the tail, hind limb and brain tissues during TH-induced and sponta

28 injury are primarily isolated to the injured hind limb and do not result in a bilateral alteration in

29 ligation, selectively homed to the ischemic hind limb and expressed IL-16.

30 ovo appearance of digit I polydactyly in the hind limb and transformations of the vertebrae.

31 s therapeutically effective both in ischemic hind limb and wound-healing models, significantly improv

32 es including a clasping abnormality of their hind limbs and a habituation deficit.

33 ear, the C-/- mice exhibited weakness of the hind limbs and progressive ataxia.

34 response and promote functional recovery in hind-limb and cardiac ischemia in animal models; however

35 howed motor dysfunctions such as weakness of hind-limb and gait abnormality in an age-dependent manne

36 nocompetent donor cells transferred with the hind limb, and (2) inactivating these cells with irradia

37 increased capillary density in the ischemic hind limb, and increased soluble Kit ligand plasma level

38 y penetrant polysyndactyly in their fore and hind limbs, and partially penetrant abnormalities of too

39 Compared to normotensive hind limb arteries (HLAs) hypertensive forelimb arteries

40 y show well-developed flight feathers on the hind limbs as well as the front limbs.

41 s, breathing irregularities, weight changes, hind limb atrophy, and scoliosis.

42 age of tetrapods and, indeed, a trend toward hind limb-based propulsion have antecedents in the fins

43 Rats were injected with bilateral hind-limb biosensors and were simultaneously subjected t

44 nitrite therapy completely restored ischemic hind limb blood flow compared with nitrate or PBS therap

45 holine uptake in the tumor and muscle and on hind limb blood flow.

46 dium nitrite significantly restored ischemic hind-limb blood flow in a time-dependent manner, with lo

47 njury of the left ventricle and simultaneous hind limb bone marrow aspiration or soleus muscle biopsy

48 lumbar and sacral vertebrae, under-developed hind limb bones and a kinky, shortened tail.

49 However, cetacean embryos do initiate hind-limb bud development.

50 Our data indicate that the cetacean hind-limb bud forms an AER and that this structure expre

51 ivity of the ZPA, is absent from the dolphin hind-limb bud.

52 36 genes differentially expressed in a mouse hind limb burn model and identify expression pattern cha

53 tion, they selectively homed to the ischemic hind limb but were unable to recruit CD4+ mononuclear ce

54 th ataxia; 2, knuckle walks; 3, movements in hind limbs but unable to knuckle walk; 4, no movement, d

55 ve neurologic phenotype including hunchback, hind limb clasp, reduced survival and brain and cortical

56 ral deficits on the accelerating rotorod and hind limb clasping tests in transgenic HD mice.

57 vere neurobehavioral abnormalities including hind limb clasping, overt seizures, motor impairment and

58 ge of phenotypes including ataxia, front and hind limb clasping, reduced brain size, and smaller neur

59 They also exhibited reduced body weight and hind limb clasping.

60 tionally, Kcne3(-/-) mice exhibited abnormal hind-limb clasping upon tail suspension (63% of Kcne3(-/

61 pid levels, and a neuromuscular abnormality (hind-limb clasping).

62 ited motor and/or behavioral defects such as hind limb clenching, reduced grip strength, and reduced

63 als distributed their weight equally between hind limbs compared to PBS-treated or untreated animals

64 cyclosporine A (CsA) to induce tolerance for hind limb composite tissue allograft in rats without chr

65 cific tolerance in the recipients of the rat hind limb composite tissue allografts.

66 induction of donor-specific tolerance in rat hind-limb composite tissue allografts using a alphabeta-

67 flow restoration in the previously ischemic hind limb, consistent with the development of angiogenes

68 collagen content and fibrosis, and decreased hind limb contractures.

69 vessels of a reduced size osteomyocutaneous hind limb CTA were anastomosed to recipient common carot

70 e units are present in diaphragm muscles and hind limb derived primary cultures of double knock out m

71 Both doses alleviated hind limb digital sensory, but not sciatic motor, nerve

72 FP15 treatment corrected sciatic motor and hind-limb digital sensory nerve conduction deficits and

73 c motor nerve conduction velocity (MNCV) and hind-limb digital sensory nerve conduction velocity (SNC

74 mb embryonic digits relative to mouse or bat hind limb digits.

75 Comparing hind limb element length, midshaft width, and robusticit

76 we analysed how the dimensions of the major hind limb elements in subfossil and modern species scale

77 a keen predatory lifestyle, including robust hind limb elements modified for grip strength.

78 pression may account for the further loss of hind-limb elements that occurred near the origin of the

79 d oil applied to any site on the ipsilateral hind limb enhanced both flexor reflexes, whereas the MG

80 Australopithecus evinced longer hind limbs, extended limb posture, and a stiff midfoot,

81 Noxious somatic afferent input from the hind limb facilitates visceral hyperalgesia, which is du

82 enhanced diabetic BMC retention in ischemic hind limbs followed by improved blood perfusion, capilla

83 illary density, but the revascularization of hind limb following ischemic surgery was significantly i

84 so stimulated cell proliferation in cultured hind limbs from early prometamorphic tadpoles, as measur

85 tocyte-specific Phd2 knockout also protected hind limbs from ischemia injury.

86 o U46619 was attenuated in isolated perfused hind limbs from mutant mice.

87 This effect translates into reductions in hind limb functional impairment.

88 No modern vertebrate has hind limbs functioning as independent, fully developed w

89 rivals by performing both vocalizations and hind limb gestural signals, called "foot flags." Foot fl

90 parable arterial insulin and glucose levels, hind-limb glucose uptake increased 2.4-fold after inhala

91 Hind limb grafts harvested with a 100 cm(2) cutaneous pa

92 on, and fibrosis, and significantly improved hind limb grip strength in mdx mice.

93 rea, endomysial collagen III deposition, and hind limb grip strength.

94 At 6 and 12 wk postsurgery, the hind limb had significantly less bone mineral density th

95 development of the vertebral column and the hind limbs has threshold signalling properties.

96 e have myotonia and suffer from intermittent hind-limb immobility attacks.

97 In vivo, hind-limb immobilization of Sprague-Dawley rats up-regul

98 Animals were divided to have one hind limb immobilized (n = 129) or sham-immobilized (n =

99 In the ischemic hind limb, implantation of myoblasts transduced to expre

100 e, joint, and skeletal muscle tissues of the hind limbs in both outbred CD-1 mice and adult C57BL/6J

101 Forelimbs and hind limbs in conditional knockout (CKO) mice were short

102 preted differently by the fore limbs and the hind limbs; in the absence of the second domain there is

103 ase abolished neovascularization in ischemic hind limb induced by eNOS gene transfer.

104 ere injected into the vastus medialis of one hind limb (INJ); the contralateral limb (NINJ) served as

105 At day 5, hind limbs injected with ECFC + MPC showed greater blood

106 ic mice but recovered to normal levels after hind-limb injection of bone marrow-derived EPCs.

107 Transection of the sciatic nerve prior to hind-limb inoculation diminished viral spread to the spi

108 ice survived at a higher frequency following hind-limb inoculation with sigma1s-null virus than when

109 In the present study, we show that hind limb intramuscular (IM) injection of alphaS can ind

110 iatic infection resulted in paralysis of the hind limb ipsilateral but not contralateral to the injec

111 jury; and increased metabolic activity after hind limb IR injury in a murine model of type-II diabete

112 Spinalized rats that receive shock when 1 hind limb is extended (contingent shock) exhibit an incr

113 ion have deficient angiogenesis in models of hind limb ischaemia and tumour-implant growth.

114 (WT) and TNFR2/p75 knockout (p75KO) mice to hind limb ischemia (HLI) surgery.

115 We used a murine model of hind limb ischemia (HLI), coupled with laser Doppler per

116 ce exhibited reduced revascularization after hind limb ischemia and tumor angiogenesis in oncogene-in

117 db/db mice underwent 1.5 hours of hind limb ischemia followed by 1, 7, or 24 hours of repe

118 ardial infarction and restored blood flow in hind limb ischemia in mouse models.

119 wild-type FvB/N mice and induced unilateral hind limb ischemia in the wild-type animal.

120 Hind limb ischemia led to an increase in MEK1 and JNK1 a

121 Hind limb ischemia model and aortic capillary sprouting

122 nalysis, enzyme and receptor inhibitors, and hind limb ischemia model in caspase-1 knock-out (KO) mic

123 , cells were directly implanted into a mouse hind limb ischemia model to test angiogenic-vasculogenic

124 w of this divergent receptor function in the hind limb ischemia model, AdipoR1- and AdipoR2-deficient

125 In a hind limb ischemia model, CD31(+) cell transplantation a

126 In a hind limb ischemia model, leukocyte accumulation in MK(-

127 EC proliferation and angiogenesis in a mouse hind limb ischemia model.

128 ngiogenesis in nonretinal models such as the hind limb ischemia model.

129 ypothesis that PARP inhibition will modulate hind limb ischemia reperfusion (IR) in a mouse model of

130 After hind limb ischemia surgery Glrx TG mice demonstrated imp

131 Immediately after hind limb ischemia surgery, the db/+ and db/db mice were

132 By applying unilateral hind limb ischemia to transgenic and wild-type mice, we

133 Unilateral hind limb ischemia was conducted in 12- to 14-week-old d

134 Mice with hind limb ischemia were divided into 6 groups: db/+, db/

135 c tissue VEGF-A levels, and flow recovery to hind limb ischemia were impaired in myeloid-specific Myh

136 n-deficient mice were analyzed in a model of hind limb ischemia where blood flow is surgically disrup

137 In a rat model of hind limb ischemia, adenovirus-mediated delivery of huma

138 arly after myocardial ischemia but not after hind limb ischemia, indicative of an important role for

139 T imaging NPR-C receptor in a mouse model of hind limb ischemia-induced angiogenesis.

140 ndothelial cells (ECs) from ROS imbalance in hind limb ischemia-subjected ob/ob mice.

141 ted neovascularization in an animal model of hind limb ischemia.

142 in immunodeficient mouse hosts with induced hind limb ischemia.

143 onance (MR) angiography in a rabbit model of hind limb ischemia.

144 he extent of revascularization in a model of hind limb ischemia.

145 number in the bone marrow and spleen during hind limb ischemia.

146 demonstrate enhanced revascularization after hind limb ischemia.

147 in vivo revascularization in the setting of hind limb ischemia.

148 resulting in attenuated revascularization in hind limb ischemia.

149 ls were higher than WT in eNOS KO tissues in hind-limb ischemia and cutaneous wounds.

150 In contrast, hind-limb ischemia failed to induce Rac1 farnesylation a

151 Hind-limb ischemia induced Rac1 farnesylation and activa

152 When evaluated in a mouse hind-limb ischemia model, the nanofibers increased tissu

153 activity and tissue perfusion in the murine hind-limb ischemia model.

154 of vasculogenesis (subcutaneous matrigel) or hind-limb ischemia produced by arterial occlusion in wil

155 Hind-limb ischemia was produced in mice by iliac artery

156 In a mouse model of hind-limb ischemia, delivery of these matrices resulted

157 hown to significantly block tissue damage in hind-limb ischemia-reperfusion injury by up to 30% in co

158 s, following the surgical induction of mouse hind-limb ischemia.

159 al vessel growth and blood flow in models of hind-limb ischemia.

160 -) mice compared with WT mice in response to hind-limb ischemia.

161 1Met) segregates with tissue protection from hind-limb ischemia.

162 utation of the distal limb when subjected to hind-limb ischemia.

163 ly Met81 or Ile81, and subjected the mice to hind-limb ischemia.

164 one, or vehicle alone were injected into the hind limb ischemic muscle one day after ligation of femo

165 ipoR1- and AdipoR2-deficient mice to chronic hind limb ischemic surgery.

166 mproves angiogenesis and blood flow in mouse hind limb ischemic tissues.

167 (+) cells isolated from ischemic muscle in a hind-limb ischemic C57BL/6 mouse model play a role in ve

168 tail autotomy, characterized by more flexed hind limb joints.

169 including our large linear bodies, elongated hind limbs, large energy-expensive brains, reduced sexua

170 uding truncated forelimbs and the absence of hind limbs, largely phenocopying existing knockouts in w

171 letion occurred earlier in forelimbs than in hind limbs, leading additionally to soft tissue syndacty

172 ular survival and arteriogenesis in ischemic hind limbs, leading to the accelerated recovery of hindl

173 ollateral flow restoration in a model of rat hind limb ligation.

174 12 h for 5 days) markedly enhanced long-term hind limb locomotion relative to that of controls.

175 no Shh activity in the fore limb, and in the hind limb low levels of Shh lead to a variant digit patt

176 emonstrate lymphatic isolation in a model of hind limb lymph node (LN) excision, consisting of ipsila

177 forelimb-dominated swimmers that used their hind limbs mainly for maneuverability and stability.

178 Hind limb maximum applied force was determined using a v

179 ation, and long-term OVL are detrimental for hind limb mdx mouse muscle, a murine model of Duchene mu

180 In a rabbit hind limb model of vascular insufficiency, intramuscular

181 ectin-mediated vascular responses in a mouse hind limb model of vascular insufficiency.

182 To assess variation in hind limb morphology, we analysed how the dimensions of

183 sion in M83 alphaS transgenic mice following hind limb muscle (intramuscular [i.m.]) injection of alp

184 d SOD1(G93A) mice show marked improvement in hind limb muscle function and motoneuron survival in the

185 ermanent female gravidity and increased male hind limb muscle mass.

186 utively active form of HIF-1alpha into mouse hind limb muscle was sufficient to increase plasma IL-10

187 Del-1 expressed in mouse or rabbit ischemic hind-limb muscle by gene transfer rapidly promotes new b

188 contractile force with repetitive stimuli of hind-limb muscle, both in vivo and in vitro, this was ab

189 rus serotype 6 (AAV6) expressing siPTEN into hind limb muscles at postnatal day 1 in SMNDelta7 mice l

190 to elucidate the source of myoblasts for all hind limb muscles in the chick and define the distinct p

191 we measured electromyogram (EMG) activity in hind limb muscles of SOD1G93A mice.

192 by (31)P magnetic resonance spectroscopy in hind limb muscles of wild-type and CA III knockout mice

193 HX), implantation of EMG wires into selected hind limb muscles, and/or injections of tracer dyes into

194 o unstressed diaphragm is higher compared to hind limb muscles, which is probably attributable to con

195 erent shRNAs were injected one time into the hind limb muscles.

196 on, in contrast to what has been reported in hind limb muscles.

197 ed motor neurons not only reinnervated lower hind-limb muscles but also enabled their function to be

198 icrospheres to measure the blood flow to the hind-limb muscles, and other body tissues, in guinea fow

199 ximately 15 ml min(-1) g(-1), and one of the hind-limb muscles, approximately 9 ml min(-1) g(-1), wer

200 ic contraction (EC)-induced injury of murine hind-limb muscles.

201 tabilize the knee and work production by the hind-limb muscles.

202 -like macrophages in the proximal and distal hind-limb muscles.

203 articipation in the development of the avian hind limb musculature and contribute to both primary and

204 type, in which androgen receptor (AR) in the hind limb musculature is expressed at levels approximate

205 increased androgenic sensitivity within the hind limb musculature.

206 tor expressing follistatin (rAAV:Fst) to the hind-limb musculature of mice two weeks prior to denerva

207 nd Ca(2+) in dystrophic muscle fibers of the hind-limb musculature predicts a net Ca(2+) influx state

208 nsgene induced dystrophy-like disease in all hind-limb musculature, as well as exacerbated the muscle

209 e Committee were used to examine ex vivo the hind limb of a rat and the toe of a pig.

210 d soft-tissue trauma was applied on the left hind limb of pentobarbital-anesthetized rats.

211 The toxin was inoculated into one hind limb of young adult rats.

212 ar CD68(+) cell infiltration in the ischemic hind limbs of diabetic mice.

213 operation, showed exacerbated disease in the hind limbs of NCX1 TG mice, similar to treatment with th

214 umor model with VX2 tumors implanted on both hind limbs of rabbits and investigated the feasibility t

215 ith emergence of mechanical allodynia in the hind limbs of rats.

216 increased capillary density in the ischemic hind limbs of wild-type mice, and this was associated wi

217 l imaging are achieved at 1-3 mm deep in the hind limb owing to the beneficial NIR-II optical window

218 tional knockout mice suffer from progressive hind limb paralysis and ataxia and die around 6 weeks af

219 ue viruses caused severe genital disease and hind limb paralysis in 129 mice, but infection of IFN-al

220 of Foxo1 resulted in exocrine pancreatitis, hind limb paralysis, multiorgan lymphocyte infiltration,

221 ival even after the mice developed bilateral hind limb paralysis.

222 henotype with ataxia, kyphotic posturing and hind limb paralysis.

223 n in axons, loss of large caliber axons, and hind limb paralysis.

224 se muscle and that are associated with fatal hind limb paralysis.

225 Gait deficits progress to complete hind-limb paralysis and death at age ~8 mo.

226 ractivity, beginning at 16 days, followed by hind-limb paralysis and death.

227 aperitoneally to mice caused weight loss and hind-limb paralysis followed by death.

228 stnatal growth rate and delayed the onset of hind-limb paralysis.

229 neurological symptoms including tremors and hind-limb paralysis.

230 intercepts with lower scaling exponents than hind limb parameters.

231 eletion of the Slc8a1 (NCX1) gene diminished hind-limb pathology in Sgcd(-/-) mice.

232 ated human endothelial cells, which enhanced hind limb perfusion (P<0.05 at day 7 and 14 after transp

233 ek dietary period, animals were subjected to hind limb perfusions in the presence (n=8 per group) or

234 hNF-L(E397K) mice, and consisted of aberrant hind limb posture, digit deformities, reduced voluntary

235 the surgical removal of lymph nodes from rat hind limbs prevented the development of lethal graft-ver

236 lateral and basolateral amygdala and in the hind limb primary somatosensory (S1HL) cortex.

237 Coordinated motor function and hind limb reflex recoveries also were improved significa

238 ncluding spastic paresis, fore limb tremors, hind limb rigidity, and a reduced life span (60-65 days

239 ession was determined from single aortas and hind limb RNA by fluorescence reverse transcription-PCR.

240 Histologic analysis of hind limb sections revealed severe necrotizing myositis,

241 Hind limb sections were stained with hematoxylin and eos

242 ibrils on the tissue level and ultimately in hind limb/segment paralysis.

243 athic pain model, LC(:SC) activation reduced hind-limb sensitisation and induced conditioned place pr

244 logical and developmental data suggests that hind-limb size was reduced by gradually operating microe

245 ssion did not drive the initial reduction in hind-limb size.

246 mposition of inflammatory infiltrates within hind limb skeletal muscle tissue.

247 performed in vivo (31)P NMR spectroscopy on hind limb skeletal muscle, to noninvasively measure high

248 morphology (XROMM) to image and animate the hind limb skeleton of a chicken-like bird traversing a d

249 pmental control genes eliminated most of the hind-limb skeleton.

250 After hind limb skin incision, Adm messenger RNA expression wa

251 their axons causes neuropathy that leads to hind limb spasticity and premature death.

252 instem, peripheral nerves from both fore and hind limbs, stifle synovium and perisynovial adipose tis

253 density of microcirculation in the ischemic hind limb, suggesting the mechanism of efficacy of this

254 Myogenic Akt signaling or ischemic hind limb surgery led to the induction of Fstl1 in muscl

255 At day 7, unilateral hind-limb surgery with excision of the left femoral arte

256 atomas contained no more cardiomyocytes than hind-limb teratomas, suggesting lack of guided different

257 ipedal but retained ape-like features in the hind limb that would have limited their walking economy

258 g, pennaceous feathers attached to the lower hind limbs (that is, 'hindwings').

259 In ischemic hind-limb tissue, skeletal muscle blood flow and arterio

260 clonal analysis of individual cells of mouse hind limb tissues devoid of nerve supply during regenera

261 presumed tissue stem/progenitor cells within hind limb tissues remain largely intact independent of n

262 e enhanced capillary density in the ischemic hind-limb to a similar extent as bFGF.

263 oxygenation challenges, including transient hind-limb tourniquet occlusion.

264 active hyperoxia occurs following release of hind-limb tourniquet occlusions.

265 The ORT hind limb transplant model seems to be best suited to st

266 -versus-host disease (GVHD) after allogeneic hind limb transplantation to chimeric recipient rats.

267 s for orthotopic (ORT) and heterotopic (HET) hind limb transplantation.

268 udy and prevent GVHD in a mixed chimeric-rat hind-limb transplantation model.

269 Hind limb transplantations were performed in Lewis-Brown

270 Orthotopic hind-limb transplantations were performed in male Lewis

271 imaging, using two morphologically different hind-limb tumor models and drug-induced alterations in a

272 Ultrasound-mediated gene delivery to mouse hind limb tumors was performed in vivo (n = 24) with ins

273 o neutral MBs in both cell culture and mouse hind limb tumors.

274 in mice with Lewis lung carcinoma and GL261 hind limb tumors.

275 carcinoma or glioblastoma multiform (GL261) hind limb tumors.

276 In hind limb U87MG xenografts, temozolomide produced a 6.4-

277 Hind limb unloading by tail suspension reduced bone mass

278 Seven days of hind limb unloading led to a 10-fold activation of an NF

279 In Col1a1-caPPR transgenic (Tg) mice, hind limb unloading suppressed bone formation parameters

280 Hind limb unloading, sciatic nerve denervation, starvati

281 on in rat soleus muscles due to 1-14 days of hind limb unloading.

282 s research revealed that OPN is critical for hind limb-unloading induced lymphoid organ atrophy throu

283 teolytic tumors throughout the vertebrae and hind limbs, using biodistribution studies and small-anim

284 ticular relevance to baroreflex function and hind limb vascular arterial reactivity to constrictor ag

285 creased alcohol consumption impairs ischemic hind limb vascular repair.

286 nificant changes in arterial blood pressure, hind limb vascular resistance and heart rate.

287 o real-time epifluorescence imaging of mouse hind limb vasculatures in the second near-infrared regio

288 The inoculated hind limb was paralysed within 3 h, and remained paralys

289 ilateral ACL transection (ACLT) of the right hind limb was performed in Lewis rats (n = 56).

290 hich a portion of the sciatic nerve from one hind limb was transected at postnatal day 8 to cause par

291 Angiogenic repair of ischemic hind limbs was impaired in adiponectin-KO mice compared

292 ic inflammatory myopathy (CIM) consisting of hind limb weakness and inflammation.

293 In a separate study, serial images of hind limbs were evaluated in 2 treatment groups: murine

294 BALB/c hind limbs were transplanted to BALB/c or C57BL6 recipie

295 Leptin induced growth and development of the hind limb, where LR mRNA is expressed.

296 165b inhibited revascularization of ischemic hind limbs, whereas treatment with an isoform-specific n

297 abbits underwent ACLT or sham surgery on one hind limb, while each contralateral limb was the nonoper

298 Gerbils were intradermally inoculated in the hind limb with 100 B. pahangi L3, and necropsies were pe

299 nvestigated by studying the effects on three hind limb withdrawal reflexes of an acute noxious stimul

300 ut was directed to the active muscles of the hind limbs, without redistribution of blood flow from th