ライフサイエンスコーパス: atropine

1 nts (control, 5 microgm and 10 microgm/kg of atropine).

2 ity upon scruffing, abrogated by infusion of atropine.

3 cholinergic antagonists, D-tubocurarine and atropine.

4 fter peak intravenous infusion of dobutamine/atropine.

5 ked by the muscarinic antagonist, 1-5 microM atropine.

6 aphysiologic doses and frequent re-dosing of atropine.

7 this was unaffected by co-administration of atropine.

8 ylamine but not by the muscarinic antagonist atropine.

9 s (20-30 s), the latter two being blocked by atropine.

10 carinic receptor antagonists pirenzepine and atropine.

11 ne of which in each case was pretreated with atropine.

12 th 1-2 ms pulses was not inhibited by TTX or atropine.

13 types of distension, before as well as after atropine.

14 ude that was not observed during exercise or atropine.

15 and this excitatory effect was abolished by atropine.

16 ability with either anesthetic agent or with atropine.

17 alteration of alpha-synuclein was blocked by atropine.

18 tment with the i.c.v. muscarinic antagonist, atropine.

19 ls is inhibited by the muscarinic antagonist atropine.

20 sphorylation of ACK-1 which was inhibited by atropine.

21 l side effects compared with higher doses of atropine.

22 r stimulation as all effects were blocked by atropine.

23 ater in eyes that had received 0.5% and 0.1% atropine.

24 e asystolic reflex by means of 0.02 mg/kg IV atropine.

25 s were blocked by the muscarinic antagonist, atropine.

26 ntagonist gabazine, and both were blocked by atropine.

27 Atropine 0.01% also caused minimal pupil dilation (0.8 m

28 yopia during phase 2 (washout), resulting in atropine 0.01% being most effective in reducing myopia p

29 Over 5 years, atropine 0.01% eyedrops were more effective in slowing m

30 east 1 eye) during phase 2 were restarted on atropine 0.01% for a further 24 months (phase 3).

31 Atropine 0.01% had a negligible effect on accommodation

32 Atropine 0.01% has minimal side effects compared with at

33 be minimized by using low doses (especially atropine 0.01%).

34 , 59%, and 68% of children originally in the atropine 0.01%, 0.1%, and 0.5% groups, respectively, who

35 ed with less rebound myopic progression (for atropine 0.01%, mean myopic progression after treatment

36 who progressed in phase 2 were restarted on atropine 0.01%.

37 c children, 6 to 12 years of age, to receive atropine 0.5%, 0.1% or 0.01% for 24 months, after which

38 .60, -0.38+/-0.60, and -0.49+/-0.63 D in the atropine 0.5%, 0.1%, and 0.01% groups, respectively (P=0

39 ssation of 0.28+/-0.33 D/year, compared with atropine 0.5%, 0.87+/-0.52 D/year), fewer side effects,

40 Perfusion with atropine (0.003 mg ml(-1)) reduced sweating below baseli

41 ses to parasympathetic withdrawal induced by atropine (0.02 mg/kg) were compared in 50 healthy subjec

42 mg/kg of acepromazine was given, and either atropine (0.2 mg) or saline was given by intravenous bol

43 R compared to its final level after systemic atropine (0.5 mum).

44 Lower dosages of atropine (0.5%, 0.1%, and 0.01%) were found to be slight

45 of CCh on VFT was abolished by a muscarinic (atropine, 0.1 mumol l(-1) , n = 6) or a nicotinic recept

46 s were -0.05 D, 0 D, -1.05 D for the 0.125 % atropine, 0.25 % atropine and control groups, with both

47 mmHg, -1.28 mmHg, -0.33 mmHg for the 0.125 % atropine, 0.25 % atropine and control groups.

48 and visual side effects of 3 lower doses of atropine: 0.5%, 0.1%, and 0.01%.

49 6/7) and significantly reduced the VA score (atropine: 0.6+/-0.2 versus vehicle: 1.7+/-0.3; P<0.05).

50 e Treatment of Myopia 1 (ATOM1), showed that atropine 1% eyedrops were effective in controlling myopi

51 the placebo group and -0.28+/-0.92 D in the atropine 1% group.

52 d of 400 children were randomized to receive atropine 1% in 1 eye only in this institutional study.

53 sting with mydriatic agents (tropicamide and atropine 1%) caused significant increases in IOP (35% an

54 muscarinic acetylcholine receptor antagonist atropine (1 microm) (103.4 +/- 3.0%), and became more fr

55 Atropine (1 microM) abolished sEJPs.

56 Atropine (1 microM) abolished the ascending excitatory r

57 In the presence of atropine (1 microM) and prazosin (100 nM), pyridoxalphos

58 iophysical changes were reversed with either atropine (1 microM) or pirenzepine (1 microM).

59 olinergic rapid oscillations were blocked by atropine (1 microm) or tetrodotoxin (1 microm).

60 in (1 microM), hexamethonium (300 microM) or atropine (1 microM), suggesting that the neural control

61 ; 0.6 microM), hexamethonium (100 microM) or atropine (1 microM), when added selectively to the stimu

62 Pretreatment of oocytes with atropine (1 micromol/L) or acetylcholine (10 micromol/L)

63 Atropine (1 muM) reduced the evoked responses in ICC-MY,

64 for isoproterenol (-0.83 +/- 0.53) than for atropine (-1.45 +/- 0.21) or exercise (-1.37 +/- 0.23) (

65 plified the increase in ACh caused by giving atropine (10 microM in the aCSF); atropine alone increas

66 CCh responses were blocked by atropine (10 mum) or 4-DAMP (100 nm), an M(3) receptor a

67 olarization were reduced or eliminated after atropine (10 mumol/L) or ranolazine (10 mumol/L).

68 nt with tetrodotoxin (TTX) (10(-6) mol/L) or atropine (10(-5) mol/L) markedly reduced 5-HT-stimulated

69 Ca2+]o, 1 micromol/L verapamil, 1 micromol/L atropine, 10 micromol/L L-N5-(1-iminoethyl)ornithine, 10

70 The muscarinic receptor antagonist, atropine (100 microM), did not alter significantly the e

71 sAPs were abolished by NF449, insensitive to atropine (126 +/- 39%) and increased in frequency by LTX

72 Following injection of atropine (15 microg kg-1, I.V.), the oesophageal distens

73 ceptor antagonist) and strongly inhibited by atropine (1microm).

74 receptors were blocked by hexamethonium and atropine, 20 Hz stimulation for 10 s initiated a sEPSP i

75 ration of the muscarinic receptor antagonist atropine (30 and 60 microg/side).

76 longer than that during exercise (330 ms) or atropine (339 ms) (p < 0.0001).

77 administered muscarinic receptor antagonist atropine (400 microA cm-2, 45 s, 10 mM) in heated subjec

78 tion was fully corrected by pertussis toxin, atropine (a nonselective muscarinic antagonist), or meth

79 Atropine, a nonselective M-type antagonist, is used in t

80 In combination with atropine, a single dose of galantamine administered befo

81 beta-blockade blunted this response whereas atropine abolished atrial fibrillation inducibility.

82 We propose that inhibition of PDE4 by atropine accounts, at least in part, for the induction o

83 -tubocurarine (D-TC), hexamethonium (C6) and atropine.ACh, nicotine and pilocarpine potentiated the e

84 esterase (PDE) activity assays, we show that atropine acts as an allosteric PDE type 4 (PDE4) inhibit

85 Atropine administration accentuated the cardiovascular r

86 dative amplitude was 11.25 +/- 0.18 D before atropine administration and 0.52 +/- 0.11 D after atropi

87 ts time course was altered by NO blockade or atropine administration when compared to pre-infusion co

88 ine administration and 0.52 +/- 0.11 D after atropine administration.

89 Atropine alone (i.e. administered without prior administ

90 by giving atropine (10 microM in the aCSF); atropine alone increased ACh concentrations from 81 to 3

91 inst NE (dibenamine or phentolamine) or ACh (atropine, alpha-bungarotoxin (alpha-BTX) or scopolamine)

92 When administered separately, only atropine ameliorated AV conduction blocks, indicating th

93 Atropine, an inhibitor of muscarinic receptors, did not

94 ting TA in 3 samples (13.9-83.9microg/kg for atropine and 5.7-10.4microg/kg for scopolamine).

95 3 receptor antagonists, but was inhibited by atropine and a 5-HT4 antagonist.

96 s heart rate was tested by pretreatment with atropine and by atrial overdrive pacing.

97 n whereas muscarine had inconsistent effects.Atropine and C6 depressed [Ca2+]i increases elicited by

98 e) and also affinity to efflux transporters (atropine and chloramphenicol) are the likely reasons for

99 D, -1.05 D for the 0.125 % atropine, 0.25 % atropine and control groups, with both atropine-treated

100 -0.33 mmHg for the 0.125 % atropine, 0.25 % atropine and control groups.

101 ring the arrest, found the administration of atropine and epinephrine to be associated with mortality

102 ers as HR increases in response to exercise, atropine and isoproterenol.

103 emergency department intubation, the use of atropine and lidocaine as premedications, the choice of

104 ta exist to determine the appropriate use of atropine and lidocaine for rapid sequence intubation.

105 by the muscarinic and nicotinic antagonists atropine and mecamylamine, respectively, in dose- and ti

106 e receptor subtype non-selective antagonists atropine and N-methylscopolamine did not.

107 urkinje fiber contractility with and without atropine and nadolol.

108 PAM, obidoxime, TMB4, or HI-6) combined with atropine and on occasion an anticonvulsant.

109 The use of adult formulated atropine and pralidoxime autoinjectors will deliver dose

110 r of age should be given a full dose of both atropine and pralidoxime from the Mark 1 kit when more a

111 Simultaneous administration of atropine and propranolol to block parasympathetic and sy

112 /-60 mmHg over 60-90 s) in rats treated with atropine and propranolol to eliminate changes in heart r

113 Solanaceae, which produce compounds such as atropine and scopolamine, this reaction is known to be c

114 The carbachol effect was blocked by atropine and SLM-driven suppression of excitatory events

115 ect was partially reversed by application of atropine and was usually not associated with significant

116 , (ii) blockade of muscarinic receptors with atropine, and (iii) facilitation of GABA(A) receptor sig

117 ysfunctional urinary bladder, for which this atropine- and P2X1 antagonist-resistant site represents

118 us alkaloids S-(-)-nicotine and hyoscyamine (atropine) are related in having a common intermediate, b

119 0.01% has minimal side effects compared with atropine at 0.1% and 0.5%, and retains comparable effica

120 ynaptic inputs during novelty was blocked by atropine at a dose that blocks type 2 theta rhythm.

121 mostly blocked by the muscarinic antagonist atropine (ATR), and the remainder by MEC.

122 Increasing doses of atropine attenuated the ethnic difference in PP (P = 0.0

123 VIP(10-28), alone or in combination with atropine, attenuated the increase in CVC during heat str

124 Increasing intrinsic sinus rate with atropine before catecholamine challenge suppressed ventr

125 (320 ADR), and (2) with vagal blockade (2 mg atropine), before and during intravenous adrenaline infu

126 Atropine blocked all contractions and all increases in p

127 The M3AChR antagonist atropine blocked the BzATP-stimulated increase in [Ca2+]

128 Atropine bolus injection (0.04 mg/kg) did not increase h

129 Secretion of insulin and PP was inhibited by atropine (both P < 0.001).

130 or-mediated mEPSCs, which was antagonized by atropine but not mecamylamine.

131 pharmacological agents such as carbachol and atropine but rarely form capillary-like structures when

132 at 20 Hz; both responses were attenuated by atropine, but only RLC phosphorylation was inhibited by

133 nduced calcium signals were not inhibited by atropine, but were abolished by caffeine or by depletion

134 ting the eye to a more myopic state and with atropine by cycloplegia.

135 However, many cardiac effects of atropine cannot be adequately explained solely by its an

136 myopic progression in children treated with atropine compared with various control groups.

137 Second, a muscarinic antagonist (atropine) completely abolished stable rhythmic activity

138 ning, associated with a negative response to atropine, could be considered immediate end points of th

139 laminar amplitude profile, are resistant to atropine, couple differently to gamma oscillations, and

140 However, like atropine, CPP blocked the habituation of synaptic modula

141 n was concentration-dependent and blocked by atropine, demonstrating mediation by muscarinic receptor

142 In vivo, the atropine-dependent prolongation of heart rate increase w

143 ence of 100 micromol/L L-NNA, 100 micromol/L atropine did not affect electrical field stimulation (EF

144 Methyl atropine did not alter NE release in the BLA in comparis

145 vel environment 48 h later in the absence of atropine did not result in habituation, but instead modu

146 nea pig vagal tissue, but glycopyrrolate and atropine did not.

147 n under 1 year of age should be given a full atropine dose from the Atropen (Meridian Medical Technol

148 The average dobutamine and atropine doses were 48 microg/kg/min and 1.2 mg, respect

149 ered an informed choice between patching and atropine drops.

150 cetylcholine, noradrenaline, propranolol and atropine, during the process of transhemispheric cortica

151 The 0.01% atropine effect, however, was more modulated and sustain

152 how that the muscarinic receptor antagonist, atropine, eliminated the effect of acetylcholine (ACh),

153 Blockade of all five mAChR subtypes with atropine evoked pronounced effects, including terminal s

154 eyedrop; 12 of them were treated with 0.25 % atropine eye drop and another 12 served as a control gro

155 roups: 32 children were treated with 0.125 % atropine eyedrop; 12 of them were treated with 0.25 % at

156 However, atropine failed to prevent or mitigate the tonic immobil

157 Children received atropine for 24 months (phase 1), after which medication

158 Topical use of low concentration atropine for one year does not induce ocular hypertensio

159 lished literature on the efficacy of topical atropine for the prevention of myopic progression in chi

160 Our previous study, Atropine for the Treatment of Myopia 1 (ATOM1), showed t

161 18 fmol/min) and in the increase produced by atropine (from 489 to 560 fmol/min; P<0.05).

162 t myopic progression compared to the 0.125 % atropine group 6 months after treatment, and persisted f

163 ct noted, with 16 cases in the 0.1% and 0.5% atropine groups, and no cases in the 0.01% group.

164 SE, or AL among the children in the various atropine groups.

165 MCh effect was blocked by atropine, guanosine-5'-O-(2-thiodiphosphate) trilithium

166 le phase than in the late contractile phase; atropine had the opposite effect.

167 Atropine has been found to be effective in the treatment

168 autonomic blockade combining propranolol and atropine has produced conflicting results.

169 The muscarinic receptor blocker atropine, however, abolished both drinking and cellular

170 bolic changes were reversed by 0.1 mg kg(-1) atropine i.v.

171 aseline in the NCE patients were reversed by atropine in a dose-dependent fashion.

172 d for the rapid detection of scopolamine and atropine in buckwheat foods.

173 xpression, inhibition of mAchR activity with atropine in innervated PM fibers induced slow MyHC2 expr

174 e with the muscarinic cholinergic antagonist atropine in random sequence.

175 relationship, was significantly higher after atropine in the isovolumic study but not in the isobaric

176 n the presence of cardiogenic shock (2D) and atropine in the presence of symptomatic bradycardia or c

177 - or M1/3-muscarinic receptor knockout mice, atropine increased cAMP levels that were pre-elevated wi

178 with the muscarinic receptor inverse agonist atropine increased cellular levels and restored both cel

179 etic influences), systemic administration of atropine increased left ventricular contractility in rat

180 uring ACh exposure, addition of 1 micromol/L atropine increased NOi production similar to ACh withdra

181 c influences), intravenous administration of atropine increases LV contractility in rats anaesthetize

182 ere mimicked by muscarine and antagonized by atropine, indicating that it requires ACh and muscarinic

183 urse of pilocarpine-induced accommodation or atropine-induced cycloplegia.

184 A was unchanged compared with baseline after atropine infusion and in the control group.

185 were obtained both before and after 1 mg/kg atropine infusion, 30 mg/kg i.v. L-NAME (N-Nitro-L-argin

186 RET)-based cAMP biosensor, we confirmed that atropine inhibited acetylcholine-induced decreases in cA

187 TTX and atropine inhibited nucleotide-evoked Isc responses.

188 Atropine inhibition produced a slow recovery or prevente

189 underwent graded-intensity bicycle exercise, atropine injection and isoproterenol infusion.

190 unteers underwent MRI tagging at rest, after atropine injection, and after exercise.

191 are blocked when animals are pretreated with atropine injections to the SCN, demonstrating that choli

192 ssion blocked, this stimulation evoked fast, atropine-insensitive EPSPs that were sensitive to nAChR

193 Atropine is a clinically relevant anticholinergic drug,

194 In comparison to exercise and atropine, isoproterenol is associated with much less QT

195 -receptor knockout mouse Langendorff hearts, atropine led to increased contractility and heart rates,

196 size and near visual acuity returned to pre-atropine levels in all groups, but accommodation at 36 m

197 SNS) and LVNS after pretreatment with methyl atropine (MA-LVNS).

198 lease were inhibited by atropine sulfate and atropine methyl bromide but not by hexamethonium.

199 sical administration of the mAChR antagonist atropine methyl nitrate (5 microM) and were absent in ra

200 e blocked by intravesical injection of 5 muM atropine methyl nitrate (AMN).

201 etylcholinesterase inhibitors and blocked by atropine methylbromide and 4-DAMP mustard, an M(3) musca

202 46 (28%) patients, symptoms persisted after atropine (mixed form), in the remaining 86 (52%) patient

203 zation with echocardiography) for dobutamine/atropine MRI for the detection of inducible ischemia wer

204 Simultaneous atropine (muscarinic antagonist) or PD142893 (endothelin

205 alpha,beta-meATP) (purinergic inhibition) or atropine (muscarinic inhibition) on neurally stimulated

206 ession revealed less myopic progression with atropine (myopic progression ranging from 0.04+/-0.63 to

207 h on VFT, an effect that was also blocked by atropine (n = 10).

208 e (esmolol, n=20), parasympathetic blockade (atropine, n=20), or no intervention (control subjects, n

209 provide sufficient evidence of an effect of atropine on myopic progression.

210 , the effect of TEA was not blocked by 10 uM atropine or by 1 mM GDPbetaS, and subsequent addition of

211 After NMB reversal, no patients received atropine or epinephrine, suffered cardiac arrest, or die

212 Atropine or inhibitors of MAPK phosphorylation blocked t

213 agonized by celiac ganglionectomy but not by atropine or N(G)-nitro-l-arginine methyl ester (L-NAME).

214 Atropine or N-methyl scopolamine treatment reduced the i

215 ital arrival, arrest rhythm not asystole, no atropine or NaHCO3, fewer epinephrine doses, shorter dur

216 d subgroups based on original treatment with atropine or patching, no significant differences were ob

217 similar regardless of initial treatment with atropine or patching.

218 In the present study, atropine or pirenzepine significantly inhibited the abil

219 nous muscarinic receptors and was blocked by atropine or proteasomal inhibitors.

220 d to the allosteric, extracellular site, and atropine or scopolamine as orthosteric building blocks,

221 Indeed, sacral application of atropine or the M2 -type receptor antagonist methoctrami

222 ract with either the orthosteric site (e.g., atropine) or a well characterized allosteric site (e.g.,

223 Data demonstrate, however, that atropine overdose is generally well tolerated in young c

224 After baroreflex blockade with atropine, PE increased blood pressure but did not change

225 ct was not influenced by pre-incubation with atropine, prazosin and propranolol, but was reversed by

226 ence was significantly higher (p = .03) with atropine premedication.

227 After bilateral vagotomy, atropine pretreatment and pre-contraction of the trachea

228 Maximal atropine pretreatment that completely blocked all the Cc

229 Since atropine prevented AEME-induced neurotoxicity, it has be

230 n pathophysiology, the muscarinic antagonist atropine reduced IIS frequency.

231 s little as 1 h or 2 h a day, and successful atropine regimens as little as one drop twice a week.

232 Thus, the atropine-resistant and cholinergic pressure contribution

233 cle pressure profile in protocol II, and the atropine-resistant pressure profiles correlated spatiall

234 mponent was reconstructed by subtracting the atropine-resistant pressures from the full pressures, re

235 onstrate that hippocampal area CA1 generates atropine-resistant theta population oscillations in resp

236 Atropine restored sinus rhythm in 5 of 5 Ex rats with AF

237 Atropine resulted in an increase in the oesophageal wall

238 Increasing the concentrations of atropine revealed that the Schild regression was curvili

239 rylation at Ser(473) of endogenous Akt in an atropine-reversible fashion.

240 ignificant positive allosteric modulation of atropine-reversible, direct-agonist-induced cellular act

241 istic tropane and other alkaloids, including atropine, scopolamine, scopoline, tropine, tropinone, an

242 This modulation is atropine sensitive and habituates in an NMDA receptor-de

243 hibit neurocardiac dysfunction manifested by atropine-sensitive atrioventricular conduction blocks an

244 tencies are markedly increased, and there is atropine-sensitive blockade of spontaneous channel openi

245 CCh (1 mum) caused atropine-sensitive depolarization and increased the maxi

246 Prolonged atropine-sensitive ictal bradycardia preceded SUDEP.

247 ic neurons/fibers caused a mecamylamine- and atropine-sensitive inward current in putative GABAergic

248 y inhibited vesicoanal reflex activity in an atropine-sensitive manner, while neostigmine (a peripher

249 t neurones in control rats showed excitatory atropine-sensitive responses to acetylcholine, and inhib

250 Similar atropine-sensitive responses were elicited by stimulatio

251 nist (-)-baclofen (5-10 microM) depressed an atropine-sensitive slow EPSP (EPSP(M)) and occluded the

252 could contribute to behaviourally relevant, atropine-sensitive, theta rhythms and link cannabinoid a

253 on of Kir2.1 by carbachol was reversible and atropine-sensitive.

254 Blocking cardiac vagal influences with atropine similarly reduced baroreflex-mediated bradycard

255 We sought to compare dobutamine-atropine stress echocardiography (DASE) and dipyridamole

256 Dobutamine-atropine stress echocardiography and DMIBI were moderate

257 Dobutamine-atropine stress echocardiography and stress-rest DMIBI w

258 ity, specificity, and accuracy of dobutamine-atropine stress echocardiography for the detection of co

259 Dobutamine-atropine stress echocardiography is an accurate test in

260 hyperemia induced by the standard dobutamine-atropine stress test is not less than hyperemia induced

261 nderwent dobutamine (up to 50 microg/kg/min)-atropine stress testing and coronary angiography.

262 waves was blocked by tetrodotoxin (TTX) and atropine, suggesting phase advancement was mediated via

263 es in adjacent ICC-MY, which were blocked by atropine, suggesting they were on the axons of excitator

264 Dry eye was induced by atropine sulfate administration and was treated with sal

265 episode requiring intravenously administered atropine sulfate and an episode of respiratory distress

266 potentiate insulin release were inhibited by atropine sulfate and atropine methyl bromide but not by

267 mblyopia of the fellow eye with patching and atropine sulfate eyedrops improves visual acuity.

268 y assigned to patching (minimum of 6 h/d) or atropine sulfate eyedrops, 1% (1 drop daily), for 6 mont

269 er combined autonomic blockade (atenolol and atropine sulfate) conditions.

270 In asystolic forms, atropine testing is able to distinguish a cardioinhibito

271 es, such as patching or blurring vision with atropine that are aimed at forcing the use of the amblyo

272 short-term collicular BF shift is blocked by atropine, the development of the long-term cortical BF s

273 tion was abolished by the muscarinic blocker atropine, the NO inhibitor N(w)-nitro-L-arginine (L-NAME

274 ed in a 2:2:1 ratio to 0.5%, 0.1%, and 0.01% atropine to be administered once nightly to both eyes fo

275 at the M2R, using the orthosteric antagonist atropine to determine unspecific binding, proved that th

276 Level I evidence supports the use of atropine to prevent myopic progression.

277 These were repeated after administering atropine to suppress the cholinergic smooth-muscle sphin

278 cal application of the muscarinic antagonist atropine to the eye, indicating that local cholinergic i

279 hese shifts are also blocked by infusions of atropine to the SCN.

280 y, we use the technique, in combination with atropine, to determine the active and passive biomechani

281 ogressed by more than 0.5 diopter (D) in the atropine-treated eye at 1 year were classified as being

282 myopia progression at 1 year was less in the atropine-treated eyes compared with the untreated fellow

283 .25 % atropine and control groups, with both atropine-treated groups showing significant myopic retar

284 Decreased PKC activity in atropine-treated innervated PM fibers correlated with sl

285 Atropine treatment reduced cardiac arrhythmias in mutant

286 sion) who may still progress while receiving atropine treatment.

287 Nicardipine, atropine, TTX, or hexamethonium (100 microM) also blocke

288 ith the antimuscarinic drugs scopolamine and atropine was able to greatly suppress novelty-induced Fo

289 % protein) during which a primed infusion of atropine was administered for 120 min at the following d

290 In Experiment 2, methyl atropine was given 10 min before VNS to assess whether s

291 In other studies, 10(-6) M atropine was perfused alone followed by 10(-7) M carbach

292 There was a myopic rebound after atropine was stopped, and it was greater in eyes that ha

293 Pilocarpine and atropine were applied topically to manipulate resting re

294 icrog/kg/min at 3-min stages with or without atropine) were both performed, in random sequence, in ea

295 followed by 10(-7) M carbachol with 10(-6) M atropine, whereas fellow control eyes received carbachol

296 r isoproterenol in comparison to exercise or atropine, which were similar.

297 study is to evaluate the effects of topical atropine with different concentrations on intraocular pr

298 participated in a randomized trial comparing atropine with patching for moderate amblyopia.

299 eral studies evaluated the optimal dosage of atropine with regard to myopic progression, rebound afte

300 Initial treatment with patching or atropine with subsequent treatment at investigator discr