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

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

4 s were blocked by the muscarinic antagonist, atropine.

5 ntagonist gabazine, and both were blocked by atropine.

6 ity upon scruffing, abrogated by infusion of atropine.

7 cholinergic antagonists, D-tubocurarine and atropine.

8 fter peak intravenous infusion of dobutamine/atropine.

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

10 aphysiologic doses and frequent re-dosing of atropine.

11 this was unaffected by co-administration of atropine.

12 ylamine but not by the muscarinic antagonist atropine.

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

14 carinic receptor antagonists pirenzepine and atropine.

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

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

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

18 ude that was not observed during exercise or atropine.

19 l side effects compared with higher doses of atropine.

20 r stimulation as all effects were blocked by atropine.

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

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

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

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

25 Atropine 0.01% had a negligible effect on accommodation

26 Atropine 0.01% has minimal side effects compared with at

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

28 , 59%, and 68% of children originally in the atropine 0.01%, 0.1%, and 0.5% groups, respectively, who

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

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

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

32 .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

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

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

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

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

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

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

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

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

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

42 6/7) and significantly reduced the VA score (atropine: 0.6+/-0.2 versus vehicle: 1.7+/-0.3; P<0.05).

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

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

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

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

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

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

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

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

51 ; 0.6 microM), hexamethonium (100 microM) or atropine (1 microM), when added selectively to the stimu

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

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

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

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

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

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

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

59 amples, finding a positive sample containing atropine (11.5 ug kg(-1)), scopolamine (2.8 ug kg(-1)) a

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

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

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

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

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

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

66 on were blunted by prior injection of methyl-atropine (5 mm/50-75 nL) into the RTN.

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

68 copolamine alongside sister tropane alkaloid atropine, a known ECL interferent.

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

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

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

72 Atropine abolished the bradycardia and AV block, but the

73 Atropine abolished these responses.

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

75 Ornithine, imidazole and atropine (acetylcholine inhibitor) inhibit Mtb growth in

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

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

78 (adjusted odds ratio, 0.2; 95% CI, 0.2-0.2), atropine (adjusted odds ratio, 0.07; 95% CI, 0.06-0.08),

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

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

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

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

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

84 Atropine, an inhibitor of muscarinic receptors, did not

85 take by desiccated ticks, while injection of atropine, an mAChR-A antagonist, did not show any effect

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

87 treatment options for myopia are limited to atropine and 7-methylxanthine, which have either signifi

88 3 receptor antagonists, but was inhibited by atropine and a 5-HT4 antagonist.

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

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

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

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

93 -0.33 mmHg for the 0.125 % atropine, 0.25 % atropine and control groups.

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

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

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

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

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

99 urkinje fiber contractility with and without atropine and nadolol.

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

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

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

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

104 /-60 mmHg over 60-90 s) in rats treated with atropine and propranolol to eliminate changes in heart r

105 The LOQs for atropine and scopolamine were around 0.4 and 1.2 ug/kg i

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

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

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

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

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

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

112 0.01% has minimal side effects compared with atropine at 0.1% and 0.5%, and retains comparable effica

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

114 o 38% for scopolamine and from 17 to 44% for atropine at levels ranging from 0.18 to 18.8 and 1.2-54.

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

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

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

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

119 (320 ADR), and (2) with vagal blockade (2 mg atropine), before and during intravenous adrenaline infu

120 ephrine, vasopressin, amiodarone, lidocaine, atropine, bicarbonate, calcium, magnesium, and dextrose

121 Atropine blocked all contractions and all increases in p

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 ered an informed choice between patching and atropine drops.

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

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

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

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

148 the efficacy and safety of low-concentration atropine eye drops at 0.05%, 0.025%, and 0.01% compared

149 The 0.05%, 0.025%, and 0.01% atropine eye drops reduced myopia progression along a co

150 reducing hours of patching and frequency of atropine eye drops with clinical success of about 83%.

151 :1 ratio to receive 0.05%, 0.025%, and 0.01% atropine eye drops, or placebo eye drop, respectively, o

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

153 esults demonstrated the superior efficacy of atropine eyedrops; 1% atropine vs placebo (change in ref

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

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

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

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

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

159 e and it is potential to detect and quantify atropine from a wide range of samples directly from herb

160 18 fmol/min) and in the increase produced by atropine (from 489 to 560 fmol/min; P<0.05).

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

162 6+/-0.90 mm and 0.43+/-0.61 mm in the 0.025% atropine group, 0.49+/-0.80 mm and 0.23+/-0.46 mm in the

163 03+/-1.02 mm and 0.58+/-0.63 mm in the 0.05% atropine group, 0.76+/-0.90 mm and 0.43+/-0.61 mm in the

164 49+/-0.80 mm and 0.23+/-0.46 mm in the 0.01% atropine group, and 0.13+/-1.07 mm and 0.02+/-0.55 mm in

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

166 .81+/-0.53 D in the 0.05%, 0.025%, and 0.01% atropine groups, and placebo groups, respectively (P < 0

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

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

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

170 Atropine has been found to be effective in the treatment

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

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

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

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

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

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

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

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

179 und hallucinogenic alkaloids scopolamine and atropine in the quids, while scanning electron microscop

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

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

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

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

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

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

186 As regards adverse events, 1% atropine induced blurred near vision (odds ratio [OR] 9.

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

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

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

190 TTX and atropine inhibited nucleotide-evoked Isc responses.

191 Atropine inhibition produced a slow recovery or prevente

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

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

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

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

196 lished the bradycardia and AV block, but the atropine-insensitive tachycardia and PVCs were abolished

197 Atropine is a clinically relevant anticholinergic drug,

198 Low-concentration atropine is an emerging therapy for myopia progression,

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

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

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

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

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

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

205 ost-treated with HI-6 dimethanesulfonate and atropine methyl nitrate.

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

207 46 (28%) patients, symptoms persisted after atropine (mixed form), in the remaining 86 (52%) patient

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

209 Simultaneous atropine (muscarinic antagonist) or PD142893 (endothelin

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

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

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

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

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

215 Responses were blocked by atropine or DAU 5884, but not AF-DX 116.

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

217 Atropine or inhibitors of MAPK phosphorylation blocked t

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

219 Atropine or N-methyl scopolamine treatment reduced the i

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

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

222 similar regardless of initial treatment with atropine or patching.

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

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

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

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

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

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

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

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

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

232 Maximal atropine pretreatment that completely blocked all the Cc

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

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

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

236 Thus, the atropine-resistant and cholinergic pressure contribution

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

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

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

240 at the AF-Nest (AFN) ablation eliminates the atropine response and decreases RR variability suggests

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

242 Atropine resulted in an increase in the oesophageal wall

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

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

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

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

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

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

249 radycardia in conscious WKY rats, and evoked atropine-sensitive bradycardia and atenolol-sensitive ta

250 AITC inhalation evoked atropine-sensitive bradycardia in conscious WKY rats, an

251 Inhaled allyl isothiocyanate (AITC) evoked atropine-sensitive bradycardia with atrial-ventricular (

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

253 Prolonged atropine-sensitive ictal bradycardia preceded SUDEP.

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

255 Similar atropine-sensitive responses were elicited by stimulatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

270 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

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

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

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

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

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

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

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

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

279 .25 % atropine and control groups, with both atropine-treated groups showing significant myopic retar

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

281 Atropine treatment reduced cardiac arrhythmias in mutant

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

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

284 change in the intercept and slope change in atropine use (p < 0.0001).

285 s analysis was performed to assess change in atropine use after the 2010 American Heart Association g

286 -0.51D, [- 0.60 to - 0.41] in 1 year), 0.01% atropine vs control (change in refraction: -0.50D, [- 0.

287 - 1.30 to - 0.25] in 1 year), 0.025 to 0.05% atropine vs control (change in refraction: -0.51D, [- 0.

288 e superior efficacy of atropine eyedrops; 1% atropine vs placebo (change in refraction: -0.78D, [- 1.

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

290 % protein) during which a primed infusion of atropine was administered for 120 min at the following d

291 Atropine was followed by orthokeratology (axial elongati

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

293 Of the 3 concentrations used, 0.05% atropine was most effective in controlling SE progressio

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

295 Pilocarpine and atropine were applied topically to manipulate resting re

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