ライフサイエンスコーパス: phenylephrine

1 hrine, EPI), and metabolic degradation (C-11 phenylephrine).

2 uction and attenuated hypertrophy to Iso and phenylephrine.

3 vasoconstrictor effect of norepinephrine and phenylephrine.

4 FAs and induced pathological hypertrophy by phenylephrine.

5 ertension (160-170mm Hg, group 2, n=6) using phenylephrine.

6 ure was manipulated with the vasoconstrictor phenylephrine.

7 d constriction, respectively, in response to phenylephrine.

8 the alpha(1)-adrenoceptor-selective agonist phenylephrine.

9 changed by fluid percussion brain injury and phenylephrine.

10 and nuclei, and back, during 2 h exposure to phenylephrine.

11 pes, consistent with blunted constriction to phenylephrine.

12 es with hypertrophy induced by 10 micromol/L phenylephrine.

13 ation at Ser695 in the fiber pretreated with phenylephrine.

14 rdiomyocytes stimulated by angiotensin II or phenylephrine.

15 lost following alpha(1a)AR stimulation with phenylephrine.

16 >6-fluoronorepinephrine > norepinephrine >>> phenylephrine.

17 induced increased cell size was inhibited by phenylephrine.

18 nly administered alternative vasopressor was phenylephrine.

19 r influence on cortical oxygenation than did phenylephrine.

20 reduced renal oxygen delivery more than did phenylephrine.

21 s infusion of sodium nitroprusside (SNP) and phenylephrine.

22 volume expansion (saline bolus) followed by phenylephrine.

23 than those induced by equi-pressor doses of phenylephrine.

24 in BP and HR after topical administration of phenylephrine.

25 limited vascular constriction in response to phenylephrine.

26 jury in untreated, preinjury, and postinjury phenylephrine (1 microg/kg/min intravenously) treated ma

27 is that showed significant improvement after phenylephrine 10% instillation.

28 xybuprocain 0.4%, cocain 4%, tropicamide 1%, phenylephrine 10%, diclophenac 0.1% along with chloramph

29 asodilatation to ACh and vasoconstriction to phenylephrine (10(-9) to 10(-5) m) were absent at 5 days

30 o mydriatic eye drops (tropicamide [1%] plus phenylephrine [10%]).

31 at 20 to 30 minutes following application of phenylephrine, 10%, and HR decreased by 60 minutes or lo

32 r HR, and the changes in BP and HR seen with phenylephrine, 10%, are short lived.

33 Following application of phenylephrine, 10%, BP increased at 5 and 10 minutes (me

34 (100 nmol/L), endothelin-1- (10 nmol/L), or phenylephrine- (10 micromol/L) induced hypertrophic cult

35 In young mice, stimulating alpha1 ARs (phenylephrine; 10(-7) m) and alpha2 ARs (UK 14304; 10(-7

36 Phenylephrine (100 mumol/L), an alpha1 adrenergic agonis

37 Data were available for phenylephrine, 2.5%, at 20 to 30 minutes and 60 minutes

38 Thus, phenylephrine, 2.5%, is safe to use in clinical routine.

39 Phenylephrine, 2.5%, leads to no clinically relevant cha

40 After continuous infusion of phenylephrine (20 mg/kg per day) for 14 days, wild-type

41 s to tyramine (-30 +/- 3 versus -41 +/- 3%), phenylephrine (-25 +/- 4 versus -45 +/- 5%), and dexmede

42 igation and puncture, vascular reactivity to phenylephrine (3 and 30 nmol/kg) before and after 7-nitr

43 ctive ingredients: tropicamide (0.25 mg) and phenylephrine (5.38 mg).

44 hat acute treatment of cardiac myocytes with phenylephrine, a prohypertrophic stimulant, transiently

45 d pressor responses and vasoconstrictions to phenylephrine, accompanied by enhanced membrane depolari

46 Vascular response to phenylephrine, acetylcholine, and sodium nitroprusside i

47 Effective prophylactic phenylephrine administration can be associated with redu

48 example, cardiac hypertrophy in response to phenylephrine agonist infusion for 2 wk was largely blun

49 uctance (FVC) to intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (al

50 sponses to local intra-arterial infusions of phenylephrine (alpha(1)-agonist) and dexmedetomidine (al

51 yramine (evokes noradrenaline (NA) release), phenylephrine (alpha1-agonist) and dexmedetomidine (alph

52 Phenylephrine (an alpha1AR agonist) potency was greater

53 s the role and mechanisms of action by which phenylephrine, an alpha(1) -adrenergic agonist stimulati

54 wever, an equivalent hypertension induced by phenylephrine, an alpha-adrenergic agonist, did not caus

55 First, preadipocytes were treated with phenylephrine, an alpha-adrenergic receptor agonist, to

56 After pupil dilation with 2.5% phenylephrine and 1% tropicamide, ocular alignment was r

57 ced pharmaceutically by the addition of 2.5% phenylephrine and 1% tropicamide.

58 system, and concentration-response curves to phenylephrine and acetylcholine were evaluated.

59 wed altered reactivity of isolated aortas to phenylephrine and acetylcholine, as well as marked acute

60 ithdrew beta-blockers and diuretics and used phenylephrine and albumin infusion to evaluate the respo

61 erve activity, and pressor responsiveness to phenylephrine and angiotensin II during hypotensive seps

62 and restored pressor responsiveness to both phenylephrine and angiotensin II toward preseptic levels

63 Pressor responses to increasing doses of phenylephrine and angiotensin II were measured at baseli

64 ivity, restored vascular sensitivity to both phenylephrine and angiotensin II, and resulted in better

65 ity (~70%), and blunted pressor responses to phenylephrine and angiotensin II.

66 The increase in [Ca(2+)](i) caused by phenylephrine and BzATP used simultaneously or sequentia

67 support 3 previously reported associations: phenylephrine and endocardial cushion defect (odds ratio

68 citrulline reverts the hyporesponsiveness to phenylephrine and increases the vasoconstrictor effect o

69 The protein secretion in response to phenylephrine and isoproterenol showed that direct stimu

70 phy induced by hypertrophic agonists such as phenylephrine and leukemia inhibitory factor.

71 f uni-x sheep had enhanced responsiveness to phenylephrine and nitrotyrosine staining and reduced sen

72 mediating cardiac hypertrophy in response to phenylephrine and pressure overload.

73 on, vasoconstriction after exposure to 1 muM phenylephrine and released nitric oxide in a manner simi

74 Vasoconstrictor responses to phenylephrine and serotonin challenge in the thoracic ao

75 Data were synthesized by concentration of phenylephrine and time of measurement following topical

76 ated cardiomyocyte hypertrophic responses to phenylephrine and to chronic pressure overload, but it a

77 during steady-state stimulus conditions (pre-phenylephrine), and after 2 min of phenylephrine (PE; an

78 an [SE], 134.2% [5.2%] vs 100.9% [2.9%], for phenylephrine, and 156.0% [5.6%] vs 125.1% [7.5%], for s

79 gical hypertrophy induced by Angiotensin II, phenylephrine, and isoproterenol, but did not affect car

80 ation, as well as activation with carbachol, phenylephrine, and KCl, were lower in old than in young

81 blood pressure was maintained by infusion of phenylephrine, and we also measured the effects of trans

82 High tidal volume ventilation impaired phenylephrine- and acetylcholine-induced responses in pu

83 MAPK activation while completely inhibiting phenylephrine- and EGF-stimulated MAPK activation.

84 in neonatal rat ventricular myocytes blocked phenylephrine- and IGF1 (insulin-like growth factor 1)-m

85 We investigated the role of pannexins in phenylephrine- and KCl-mediated constriction of resistan

86 and [Ca(2+)]i in response to locally applied phenylephrine, Ang II, arginine vasopressin, elevated [K

87 wing transverse aortic constriction (TAC) or phenylephrine/Ang II infusion, but showed no reduction i

88 tly regulate cell response to isoproterenol, phenylephrine, angiotensin II and stretch.

89 Fetal treatment with phenylephrine, angiotensin II and vasopressin produced s

90 and tonic contractile responses elicited by phenylephrine, angiotensin II, endothelin-1, U46619, and

91 Abs did not alter the vascular reactivity to phenylephrine, angiotensin II, or acetylcholine in nativ

92 , stimulation of the alpha1aAR with low dose phenylephrine ( approximately 10(-8) M) induced an Erk-d

93 asurements were obtained by concentration of phenylephrine as a mean change and its standard deviatio

94 eduction in force development in response to phenylephrine as well as sensitizing the muscle to acety

95 and in vivo and ex vivo arterial response to phenylephrine at 18 hours after induction of murine endo

96 the time following administration of topical phenylephrine at which measurements were obtained by con

97 Phenylephrine blunted extracellular signal-related kinas

98 se profoundly enhanced vascular responses to phenylephrine both in vitro and in vivo.

99 hr-696 and Thr-853 were also stimulated with phenylephrine but significantly less than in bladder tis

100 te signals for some small molecules, such as phenylephrine, by up to 3-fold.

101 We used photolysis of caged phenylephrine, caged guanosine 5'-O-(thiotriphosphate) (

102 that alpha-adrenergic receptor activation by phenylephrine causes a transient, PKD-dependent HDAC5-GF

103 suppressed 8-pCPT-AM-mediated relaxation in phenylephrine-contracted arteries (24.8 +/- 4.9% relaxat

104 T-AM) elicited a 77.6 +/- 7.1% relaxation of phenylephrine-contracted arteries over a 5 min period (m

105 ined unchanged during time and hypertensive (phenylephrine) control experiments.

106 vasopressin/selepressin, angiotensin II, and phenylephrine could have a fundamental advantage over no

107 Phenylephrine decreased impairment of hypotensive pial a

108 Equi-pressor infusion of phenylephrine did not significantly reduce RBF or renal

109 rfusion pressure of 70 mm Hg with the use of phenylephrine early after injury in the immature brain w

110 Likewise, stimulation of the alpha1-AR with phenylephrine enhanced macrophage phagocytosis and RvD1

111 ed pressor responses, because bolus doses of phenylephrine evoked attenuated pressor responses after

112 Arginine vasopressin was as effective as phenylephrine for maintaining cerebral perfusion pressur

113 hat arginine vasopressin was as effective as phenylephrine for maintaining tissue oxygenation during

114 pupil dilation with 1 % tropicamide and 10 % phenylephrine for retinal examination, acute elevation o

115 ely and under natural viewing conditions and phenylephrine (for accommodative efforts ranging from 0

116 Stimulation of the alpha1aAR by high dose phenylephrine (>10(-7) M) induces an antiproliferative,

117 P14 activity is increased by angiotensin II, phenylephrine, GTP, and guanosine 5'-O-[gamma-thio]triph

118 Phenylephrine has been used safely in mothers with cardi

119 Topical phenylephrine hydrochloride is routinely administered wi

120 ate to a change in blood pressure induced by phenylephrine i.v. was significantly increased (610+/-17

121 ential bolus injections of nitroprusside and phenylephrine in 14 young healthy subjects.

122 bolus injections of sodium nitroprusside and phenylephrine in 22 young, 21 older sedentary and 10 old

123 thoracic aorta segments were stimulated with phenylephrine in the presence or absence of 7-nitroindaz

124 rogates the cardiomyocyte growth response to phenylephrine in vitro through inhibition of p38 and the

125 Phenylephrine increased ATP release from pieces in a tim

126 Phenylephrine increased BP by 11, 23 and 37% from baseli

127 atively, increased IP3 production induced by phenylephrine increased Ca(2+) transient and wave freque

128 based RBCK1 overexpression in the absence of phenylephrine increased cardiac cell size.

129 s in target phosphorylation at CaMKII sites: phenylephrine increases histone deacetylase 5 phosphoryl

130 Phenylephrine induced a dose-dependent contraction of WT

131 ownregulation of PDE1A using siRNA prevented phenylephrine induced pathological myocyte hypertrophy a

132 Following chronic hypoxia during pregnancy, phenylephrine induced significantly higher pressor respo

133 In primary cultured rat cardiomyocytes, phenylephrine-induced activation of nuclear factor-kappa

134 Phenylephrine-induced aortic contraction was reduced in

135 Baroreflex heart rate responses to phenylephrine-induced blood pressure elevation and IKACh

136 (CXCL12, ubiquitin) reduced the EC50 of the phenylephrine-induced blood pressure response three- to

137 heteromeric complexes in VSMC and abolished phenylephrine-induced Ca(2+) fluxes and MLC2 phosphoryla

138 PKC down-regulation attenuates phenylephrine-induced Ca(2+) wave velocity, whereas resp

139 In phenylephrine-induced cardiac hypertrophy, ang1-256 redu

140 ing postnatal development and decreased with phenylephrine-induced cardiac hypertrophy, whereas tie2

141 emodeling and overexpressed ang1 monomers in phenylephrine-induced cardiac hypertrophy.

142 For example, both AC6 and AC6mut reduced phenylephrine-induced cardiac myocyte hypertrophy and ap

143 -33 markedly antagonized angiotensin II- and phenylephrine-induced cardiomyocyte hypertrophy.

144 otenone-induced constriction while enhancing phenylephrine-induced constriction.

145 Increased phenylephrine-induced contractile response after treatme

146 reduced the ability of 8-pCPT-AM to reverse phenylephrine-induced contraction (arteries relaxed by o

147 Phenylephrine-induced contraction and nitric oxide donor

148 and late sustained phases, respectively, of phenylephrine-induced contraction, regardless of arteria

149 ic, U46619, and had no significant action on phenylephrine-induced contractions.

150 Functionally, phenylephrine-induced heterocellular calcium communicati

151 hand, Gfat1 inhibition significantly blunts phenylephrine-induced hypertrophic growth in cultured ca

152 y RNA interference technology attenuated the phenylephrine-induced hypertrophic response in cardiomyo

153 ell death, whereas Yap1 depletion attenuated phenylephrine-induced hypertrophy and augmented apoptosi

154 show that in vitro, GHRH(1-44)NH2 attenuates phenylephrine-induced hypertrophy in H9c2 cardiac cells,

155 tes compared with nonsilencing controls in a phenylephrine-induced hypertrophy model.

156 Phenylephrine-induced hypertrophy was associated with in

157 ocytes significantly inhibited and increased phenylephrine-induced hypertrophy, respectively.

158 tl1 promoted AMPK activation and antagonized phenylephrine-induced hypertrophy.

159 dogenous RBCK1 protein levels increased upon phenylephrine-induced hypertrophy.

160 e corroborated in vivo, where acute systemic phenylephrine-induced increases in blood pressure evoked

161 istically, beta3-AR overexpression inhibited phenylephrine-induced nuclear factor of activated T-cell

162 )(-) production in the nucleus and prevented phenylephrine-induced oxidation and nuclear exit of HDAC

163 A and NPPB, at basal condition and abolished phenylephrine-induced pathological gene expression.

164 NF-kappaB, it inhibited angiotensin II- and phenylephrine-induced phosphorylation of inhibitor of NF

165 We observed an inhibition of phenylephrine-induced proliferation in small cholangiocy

166 Furthermore, PDE1A plays a critical role in phenylephrine-induced reduction of intracellular cGMP- a

167 line-mediated vascular relaxation as well as phenylephrine-induced vasoconstriction.

168 crovascular oscillators were examined during phenylephrine-induced vasoconstriction.

169 -activated K(+) (BKCa) channels in buffering phenylephrine-induced vasoconstrictions was decreased, w

170 BP was increased stepwise with phenylephrine infusion at 0.5, 1.0 and 2.0 microg kg(-1)

171 Prophylactic phenylephrine infusion can cause hypertension if increas

172 = 4) underwent a separate intervention with phenylephrine infusion to independently consider the inf

173 y and related gene expression due to chronic phenylephrine infusion.

174 ertrophy following 2 weeks of angiotensin II/phenylephrine infusion.

175 uring SNP, and increased by 21 +/- 8% during phenylephrine infusion.

176 blunted mean arterial pressure responses to phenylephrine injection (55+/-10% versus 93+/-7%, P<0.05

177 Intracameral phenylephrine is a highly efficient measure for prophyla

178 Phenylephrine is often used for management of cerebral p

179 Phenylephrine is the current vasopressor of choice for t

180 s the results based on endothelin-1, because phenylephrine is thought to act exclusively through Galp

181 ric oxide, sildenafil, dopamine, dobutamine, phenylephrine, isoproterenol, and vasopressin.

182 of isolated arteries from SMTNL1 KO mice to phenylephrine, KCl-dependent membrane depolarization and

183 Phenylephrine, L-NMMA or placebo was administered on dif

184 but attenuated alpha1-adrenoreceptor agonist phenylephrine-mediated inhibition (40 microM; NORM, 36 +

185 endent mechanism, whereas isoproterenol- and phenylephrine-mediated mechanisms had a significant auto

186 h increased 20-HETE-dependent sensitivity to phenylephrine-mediated vasoconstriction and with decreas

187 In patients with good responses to phenylephrine, MMCR may offer an efficient and highly ef

188 Sequential nitroprusside and phenylephrine (modified Oxford test) were used to evalua

189 Neither phenylephrine nor haemodilution influenced NVC.

190 Neither phenylephrine nor placebo altered basal choroidal blood

191 For 120-480 mins, phenylephrine, normal saline, and dextrose were administ

192 Stimulation of myocytes with phenylephrine or angiotensinII causes GRK5 to leave the

193 After 120 mins, phenylephrine or arginine vasopressin was titrated to ce

194 Stimulation of alpha1A-AR with phenylephrine or direct activation of PKC with phorbol e

195 Stimulation of IP3 production by phenylephrine or endothelin-1 had a positive chronotropi

196 Intracameral phenylephrine or epinephrine, either by direct injection

197 nstriction (without altering the response to phenylephrine or KCl) and preventing O2-induced increase

198 easured while AP was altered by infusions of phenylephrine or nitroprusside (+/-60 mmHg over 60-90 s)

199 sized that either the alpha-receptor agonist phenylephrine or the nitric oxide synthase (NOS) inhibit

200 ontractions to the alpha1-adrenergic agonist phenylephrine or the thromboxane (TX) A2 analog U-46619

201 carbachol, the alpha(1D)-adrenergic agonist phenylephrine, or EGF.

202 s or of either the partial alpha(1)-agonist, phenylephrine, or full alpha(2)-agonist, dexmedetomidine

203 ressure and was responsive to treatment with phenylephrine (PE) (10(-5) m) and ACh (10(-5) m).

204 Similarly, arteriolar constriction with phenylephrine (PE) (10(-5) m) induced a significant incr

205 rtas from these mice were hypocontractile to phenylephrine (PE) and had increased basal NO generation

206 Functional responsiveness to phenylephrine (PE) and sodium nitroprusside (SNP) decrea

207 as stimulated with increasing bolus doses of phenylephrine (PE) following maternal vehicle or allopur

208 by 5 min) of the alpha(1)-adrenergic agonist phenylephrine (PE) in combination with 8-Br-cGMP yielded

209 nergic stimulation of H9c2 cardiomyocytes by phenylephrine (PE) increased the cell size with enhanced

210 The alpha-adrenergic agonist phenylephrine (PE) increased tissue stress and stiffness

211 y, treatment of rat mesenteric arteries with phenylephrine (PE) led to the increase in CAS tyrosine p

212 ded in dorsal finger during iontophoresis of phenylephrine (PE) or clonidine (0.5 mm, seven 0.1 mA pu

213 In isolated mesenteric arterial rings, phenylephrine (PE) produced concentration-dependent vaso

214 w microneedle (HM) was prepared to deliver a phenylephrine (PE) solution into the anal sphincter musc

215 lamines norepinephrine (NE), epinephrine, or phenylephrine (PE) than are the alpha1B and alpha1D subt

216 ated that stimulation of cardiomyocytes with phenylephrine (PE), a well known hypertrophic agonist, s

217 administration of alpha-adrenergic agonists (phenylephrine (PE), alpha(1); clonidine (CL), alpha(2)).

218 educed the vascular contractility induced by phenylephrine (PE), and caused a dose-dependent relaxati

219 phic stimuli, including isoproterenol (ISO), phenylephrine (PE), and endothelin-1 (ET-1).

220 I (Ang II) and the alpha-adrenergic agonist, phenylephrine (PE), on cardiac energy metabolism in expe

221 t induce hypertrophy, endothelin-1 (ET1) and phenylephrine (PE), trigger comparable global PKD activa

222 ith a dose-response using the alpha1-agonist phenylephrine (PE), with and without the nitric oxide sy

223 During phenylephrine (PE)-induced contraction, SNP reduced CPI-

224 omyocytes, overexpression of miR-378 blocked phenylephrine (PE)-stimulated Ras activity and also prev

225 Phenylephrine (PE)-triggered hypertrophy and autophagy i

226 infusion of an alpha-adrenoreceptor agonist, phenylephrine (PE, 0.025 to 0.8 mug kg min) and an alpha

227 ed the responses to IGF1 (10 nmol/liter) and phenylephrine (PE, 20 mumol/liter), a known GATA4 activa

228 10(9)-1 x 10(4)m), constrictor responses to phenylephrine (PE; 1 x 10(9)-1 x 10(4)m), and flow-induc

229 Contractile response to phenylephrine (PE; 10(-10) to 10(-4)M), an alpha1-adrene

230 ce (FVC) to local intra-arterial infusion of phenylephrine (PE; alpha(1) -agonist) during (i) infusio

231 atheter) to local intra-arterial infusion of phenylephrine (PE; alpha1 -adrenoceptor agonist) were ca

232 ductance (FVC) to intra-arterial infusion of phenylephrine (PE; alpha1 -agonist) during ATP or contro

233 Phenylephrine (PE; alpha1AR agonist) evoked greater (P <

234 ions (pre-phenylephrine), and after 2 min of phenylephrine (PE; an alpha1 -adrenoceptor agonist) infu

235 d by stepwise sodium nitroprusside (SNP) and phenylephrine (PhE) infusion.

236 le function develops in response to low dose phenylephrine (PHE, 100 nM) in controls, while function

237 ed with either an alpha1-adrenergic agonist, phenylephrine (PHE; 0.5 mg/kg BW), an alpha2-adrenergic

238 es, bath application of the alpha(1)-agonist phenylephrine (PHE; 10 microM) depolarized 10 of 25 neur

239 take and no washout in healthy humans; (11)C-phenylephrine (PHEN), a tracer of vesicular leakage and

240 were greater in males, which were blunted by phenylephrine pre- or postfluid percussion brain injury.

241 ne exerted a potent vasodilatatory effect on phenylephrine pre-constricted arterial rings, which was

242 acological AMPK activation by A769662 caused phenylephrine pre-constricted UtA from normoxic or hypox

243 Measurements were obtained under phenylephrine preoperatively and under natural viewing c

244 Phenylephrine prevented reductions in cerebral blood flo

245 l tissue PO2 more than equi-pressor doses of phenylephrine, probably because it reduced renal oxygen

246 Phenylephrine rapidly induced CPI-17 phosphorylation fro

247 Phenylephrine regimens need to be developed that can rel

248 Pretreatment with a vasoconstrictor, phenylephrine, resulted in a reversal of the effect of Y

249 e agents such as angiotensin II (Ang II) and phenylephrine results in an abnormally large increase in

250 sting myocardial blood flow and EPI, HED and phenylephrine retention were homogeneous in healthy volu

251 ct cardiovascular health, better evidence on phenylephrine's effects on HR and BP is required.

252 levation of cerebral perfusion pressure with phenylephrine sex dependently prevents impairment of cer

253 ncreased cerebral perfusion pressure through phenylephrine sex dependently reduces impairment of cere

254 glucagon or Ca(2+)-mobilizing agents such as phenylephrine show an increase in their adenine nucleoti

255 Mouse hearts exposed to phenylephrine show selective CaMKIIdelta activation in t

256 stance arteries were analyzed in response to phenylephrine, sodium nitroprusside, or acetylcholine wi

257 Phenylephrine stimulated small cholangiocyte proliferati

258 Phenylephrine stimulated the Ca(2+) -dependent DNA-bindi

259 Phenylephrine stimulated the production of intracellular

260 letion of ACC2 (acetyl-CoA-carboxylase 2) in phenylephrine-stimulated cardiomyocytes and in pressure

261 GATA4 and cardiac hypertrophic responses in phenylephrine-stimulated cardiomyocytes, whereas knockdo

262 ved from Fluo-4 fluorescence measurements in phenylephrine-stimulated Flp293 cells.

263 Phenylephrine-stimulated free intracellular calcium was

264 The P2X(7) antagonist A438079 blocked the phenylephrine-stimulated increase in [Ca(2+)](i) but not

265 the level of phosphorylation is increased by phenylephrine stimulation accompanied by increased level

266 Furthermore, in response to phenylephrine stimulation, PRMT5 translocates into the c

267 y the alpha-adrenergic receptor (AR) agonist phenylephrine, suggesting inhibition of alpha-AR signali

268 Washout was only observed for phenylephrine (T(1/2) 49+/-6 min).

269 of 5 mm Hg or higher in at least 1 eye; (2) phenylephrine testing identified eyes at high risk for d

270 Parma, Italy, 72 patients with PDS underwent phenylephrine testing.

271 a hypo-contractile phenotype in response to phenylephrine that was abolished when vessels were incub

272 t cardiomyocytes induced to hypertrophy with phenylephrine, the adenosine analogue 2-chloroadenosine

273 In vitro studies using phenylephrine-treated neonatal rat ventricular myocytes,

274 A prolonged phenylephrine treatment also resulted in an increase of

275 including transverse aortic constriction and phenylephrine treatment.

276 e in cell size of cardiac myocytes following phenylephrine treatment.

277 g search terms: topical, ocular, ophthalmic, phenylephrine, tropicamide, cardiovascular effect, side

278 time of measurement or the concentration of phenylephrine used were excluded.

279 However, with phenylephrine vs. arginine vasopressin, intracranial pre

280 surized thoracodorsal resistance arteries to phenylephrine was decreased significantly by multiple Pa

281 The decrease in EIVPD induced by phenylephrine was inversely related to baseline systolic

282 ient, and pupillary supersensitivity to 2.5% phenylephrine was not observed.

283 52.0%-58.4%) in the second quarter of 2011; phenylephrine was the most frequently used alternative v

284 ith trimethaphan (3-7 mg min(1)), continuous phenylephrine was titrated to restore blood pressure to

285 ensitized force and activation of RhoA, when phenylephrine was used as an agonist.

286 Phenylephrine was well tolerated and there were no obser

287 Phenylephrine washout was not different from healthy vol

288 high glucose on reactivity to carbachol and phenylephrine were determined.

289 on or volume expansion; pressor responses to phenylephrine were enhanced and baroreflexes impaired in

290 teristic aortic impedance, and reactivity to phenylephrine were similarly increased in hypertensive Z

291 Contractions evoked by ET-1(1-31), but not phenylephrine, were reduced by inhibition of cyclooxygen

292 paired contraction of vessels in response to phenylephrine, whereas MPs from healthy controls or from

293 OS)-generating hypertrophic stimuli, such as phenylephrine, whereas they are reduced by Trx1.

294 ereas defect of a third catecholamine, (11)C-phenylephrine, which is sensitive to metabolic degradati

295 o dilate rat aorta strips precontracted with phenylephrine with a NO-dependent mechanism.

296 r response to Ang II; however, coinfusion of phenylephrine with Ang II, which restored the Ang II pre

297 ll (but not large) cholangiocytes respond to phenylephrine with increased proliferation via the activ

298 hosphate (BzATP) or the alpha(1D)-AR agonist phenylephrine with or without antagonist preincubation.

299 ed vasorelaxation in UtA preconstricted with phenylephrine, with HA-UtA showing increased sensitivity

300 duced by the alpha(1)-adrenoreceptor agonist phenylephrine, without affecting activation of the ERK/R