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1 rred after local beta-adrenoceptor blockade (propranolol).
2 ta-AR antagonists (1 muM prazosin and 10 muM propranolol).
3 renoreceptor blockade (5 mM yohimbine + 1 mM propranolol).
4 (ISO), or the beta-adrenoceptor antagonist, propranolol.
5 d DR, and DH Fos was decreased by systemic S-propranolol.
6 ation was not blocked with betaAR antagonist propranolol.
7 Both are prevented by treatment with propranolol.
8 72 months) underwent treatment with systemic propranolol.
9 o better than aspirin, dihydroergotamine, or propranolol.
10 peridin-1-yl)propan-2-ol (A-core)] recalling propranolol.
11 olff-Parkinson-White, comparing digoxin with propranolol.
12 r injection; P<0.0001) and were inhibited by propranolol.
13 rence in infants treated with digoxin versus propranolol.
14 c prophylaxis of SVT in infants: digoxin and propranolol.
15 ts metabolic stability was much greater than propranolol.
16 er(24) unless the mice were pre-treated with propranolol.
17 he study, 27 randomized to digoxin and 34 to propranolol.
18 tation since these effects were abolished by propranolol.
19 TSD, but not necessarily in combination with propranolol.
20 o have poorer outcomes than those not taking propranolol.
21 All effects on the CR were wholly blocked by propranolol.
22 s effect when administered concurrently with propranolol.
23 at beta(2)AR was competitively inhibited by propranolol.
24 These effects were blocked by propranolol.
25 of high-dose (80 mg) versus low-dose (20 mg) propranolol.
26 by previous administration of yohimbine and propranolol.
27 the addition of the beta-adrenergic blocker propranolol.
28 nstable wild-type receptor by the antagonist propranolol.
29 onstants between immobilized AGP and R- or S-propranolol.
30 the addition of the beta-adrenergic blocker propranolol.
31 propranolol-d7 and varied concentrations of propranolol.
32 1 wk of oral treatment with the beta-blocker propranolol.
33 the full SERS spectral data and the level of propranolol.
34 space could be correlated with the level of propranolol.
35 ther resection of the carotid sinus nerve or propranolol.
36 and in vitro ADME-tox profiles comparable to propranolol.
37 n the placebo group and the groups receiving propranolol.
38 ) included patients initiating bisoprolol or propranolol.
39 sated cirrhosis before and after intravenous propranolol (0.15 mg/kg): 194 patients had an HVPG >/=10
41 were mitigated by systemic administration of propranolol (10 mg/kg, i.p.), a beta-noradrenergic recep
43 1), the beta-adrenergic receptor antagonist propranolol (2 mug) or vehicle (Experiment 2), or the be
44 The second patient was taking amiodarone and propranolol; 2 hrs after receiving sofosbuvir and daclat
45 h POTS (n=54) underwent acute drug trials of propranolol 20 mg orally and placebo, on separate mornin
50 nergic and 5-HT1A/1B receptor antagonist), R-propranolol (5-HT1A/1B receptor antagonist), or racemic
51 ymptoms at 2 hours was greater with low-dose propranolol (-6 versus -2 arbitrary units; P=0.041).
53 d antagonist), alone and in combination with propranolol (a beta-adrenergic blocker), both given syst
57 ive alpha-adrenergic receptor antagonist, or propranolol, a nonselective beta-adrenergic receptor ant
59 thin tissue sections from animals dosed with propranolol, adhered to an adhesive tape substrate, prov
61 RANKL expression by MSCs decreased after propranolol administration and increased after isoproter
66 ne, terbutaline, metaproterenol, salmeterol, propranolol, alprenolol, bisoprolol, ICI 118,551, and bu
70 nergic-induced arrhythmias by beta-blockers (propranolol and carvedilol), flecainide, and the neurona
72 f interaction were occurring between R- or S-propranolol and HDL at 37 degrees C: saturable binding w
73 e the true binding strength between R- and S-propranolol and HPLC columns containing immobilized AGP.
75 face sampling exemplified by the analysis of propranolol and its hydroxypropranolol glucuronide phase
76 e, provided semiquantitative information for propranolol and its hydroxyproranolol glucuronide metabo
77 tem were established using the drug molecule propranolol and its isotope labeled internal standard in
80 In sympathetic neuronal cell cultures, both propranolol and metoprolol increased axon outgrowth but
87 s, the sympathetic nervous system (SNS) with propranolol and the hypothalamic-pituitary-adrenal axis
91 g contaminants (caffeine, ciprofloxacin, and propranolol) and two model compounds (fluorescein and su
92 idine), beta-adrenergic receptor antagonist (propranolol), and beta(1)- and beta(2)-antagonist (betax
93 d by previous administration of prazosin and propranolol, and 4) epinephrine in which both alpha2- an
94 ency (HF) fraction of HRV in the presence of propranolol, and a decrease in expression of the G-prote
95 e beta1- and beta2-adrenergic receptors with propranolol, and by blocking protein kinase A with KT572
96 in vivo can be blocked with the beta-blocker propranolol, and by knockdown of RANK expression in MDA-
97 acetaminophen, ciprofloxacin, trimethoprim, propranolol, and carbamazepine (>80%) was achieved withi
99 rst cardiac events for atenolol, metoprolol, propranolol, and nadolol were 0.71 (0.50 to 1.01), 0.70
100 hotolysis rates for atenolol, carbamazepine, propranolol, and sulfamethoxazole in wetland water under
101 ums and by Ca(2+), Zn(2+), N-ethylmaleimide, propranolol, and the sphingoid bases sphingosine and sph
102 milar to the effect of the betaAR antagonist propranolol, and this effect was reversed by the mGlu3-n
103 a limit of detection of 2.36 ng/mL (7.97 nM) propranolol, and this is significantly lower (>25 times)
104 etermined limits of detection for serotonin, propranolol, and tryptophan were 51, 37, and 280 nM, res
106 550 g were administered either beta-blocker, propranolol, angiotensin converting enzyme inhibitor, ca
109 The current treatments, corticosteroid or propranolol, are administered for several months and can
113 corresponding to the decrease in transfer of propranolol at an aqueous-1,2-dichloroethane interface.
114 e combined administration of oxandrolone and propranolol at the same doses, for 1 year after burn.
116 Combined administration of oxandrolone and propranolol attenuates burn-induced growth arrest in ped
117 e of four propranolol regimens (1 or 3 mg of propranolol base per kilogram of body weight per day for
118 traditional beta-blockers (eg, atenolol and propranolol), because there are currently no mortality a
119 n of the beta-adrenergic receptor antagonist propranolol before memory retrieval, but not after (duri
120 seeking behavior on ED1 following 10 mg/kg S-propranolol (beta-adrenergic and 5-HT1A/1B receptor anta
122 were treated in counter-balanced order with propranolol (beta-AR antagonist), terazosin (alpha1-AR a
123 ules (R)-Naftopidil (alpha1-blocker) and (S)-Propranolol (beta-blocker) as a key step via AKR of sing
124 these dilatations were inhibited by 10(-7) m propranolol (betaAR antagonist) which otherwise had no e
126 drenoceptor activity with local infusions of propranolol blocked the memory retrieval impairment indu
127 ioma shrinkage is rapidly observed with oral propranolol, but a minimum of 6 months of therapy is rec
128 HMG-CoA reductase inhibitors, combined with propranolol, can cause mitochondrial toxicity, yielding
129 tting, we demonstrated that isoproterenol, S-propranolol, CGP-12177 [4-[3-[(1,1-dimethylethyl)amino]2
130 in asthma, showing no significant effect of propranolol compared with placebo on either methacholine
133 s containing the same fixed concentration of propranolol-d7 and varied concentrations of propranolol.
135 of the beta1-, beta2-adrenoceptor antagonist propranolol decreases cardiac work and resting energy ex
136 +/- 30 ml min(-1)) or combined phentolamine/propranolol (Delta213 +/- 25 ml min(-1); P < 0.05 for bo
137 bited a 6.5-times higher current density for propranolol detection due to the enhanced ion flux arisi
143 /kg/h), or a combination of phentolamine and propranolol (each 1 mg/kg/h), suggesting a need for new
144 /kg/h), or a combination of phentolamine and propranolol (each 1 mg/kg/h), suggesting a need for new
150 d to be greater for (S)-propranolol than (R)-propranolol for solutions containing constant concentrat
152 pranolol and the radioactivity attributed to propranolol from WBA sections indicated nominal agreemen
154 owever, in the placebo group, but not in the propranolol group, memory vividness significantly decrea
163 that blocking beta-adrenergic signaling with propranolol hydrochloride disrupts angiosarcoma cell sur
164 l hydrochloride, the binding of (S)- and (R)-propranolol hydrochloride to the protein results in a de
166 The patient was immediately administered propranolol hydrochloride, 40 mg twice a day, as his wor
170 before and after systemic beta-blockade with propranolol in 17 young men, 17 young women and 15 postm
171 ly relevant concentrations of metoprolol and propranolol in blood samples were measured over several
173 stem for online and absolute quantitation of propranolol in mouse brain, kidney, and liver thin tissu
174 omized placebo-controlled crossover trial of propranolol in patients with mild-to-moderate asthma rec
179 o the nucleus tractus solitarii (NTS) and by propranolol infused into the basolateral complex of the
180 We used bilateral intracranial infusions of propranolol into either the infralimbic division of the
182 high risk for subsequent cardiac events, and propranolol is the least effective drug in this high-ris
188 with small molecular changes as compared to propranolol molecule were generated by a nontargeted pho
189 of the tumor before and after only 1 week of propranolol monotherapy revealed a reduction in the prol
190 eters of 382 LQT1/LQT2 patients initiated on propranolol (n = 134), metoprolol (n = 147), and nadolol
191 e of 40 mg of the noradrenergic beta-blocker propranolol (n = 15), double-blind and placebo-controlle
194 ng the effects of the beta-adrenergic agents propranolol (non-selective beta-antagonist) and salbutam
195 The effect of the noradrenergic inhibitor propranolol on (14)C-FBnTP response to cold stimulation
196 The opposite direction of the effects of propranolol on corticomuscular coherence and tremor, and
197 s provide a plausible mechanism of action of propranolol on regression of infantile hemangiomas.
198 etreatment with 1 mg (100 g body weight)(-1) propranolol or 6 mg (100 g body weight)(-1) iopanoic aci
199 ered the beta-adrenergic receptor antagonist propranolol or a placebo before they reactivated previou
205 s underwent a 6- to 8-week dose titration of propranolol or placebo as tolerated to a maximum of 80 m
206 macological blockade of either sympathetic - propranolol - or parasympathetic - methylatropine - sign
207 beta-adrenergic antagonists phentolamine and propranolol, or 3) adrenergic blockade plus cholinergic
209 infants with periocular IH were treated with propranolol (oral) for 2-12 months (mean: 7.1 months).
210 ve HPAC columns with reproducible binding to propranolol over 4-5days of continuous operation at pH 7
212 patients on digoxin and 67% for patients on propranolol (P=0.34), and there were no first recurrence
213 s of trial treatment, the regimen of 3 mg of propranolol per kilogram per day for 6 months was select
214 nucleotides (ATP and CTP), N-ethylmaleimide, propranolol, phenylglyoxal, and divalent cations (Ca(2+)
216 rescued the IED; animals receiving intra-BLA propranolol prior to immediate extinction showed less sp
217 s after intravenous administration of either propranolol (PROP), or glycopyrrolate (GLYC), or PROP an
218 clotrimazole (CTZ), clofibric acid (CFA) and propranolol (PRP), found responses to IBU and CFA, but n
219 ng was subsequently used to provide accurate propranolol quantification within all biofluids with hig
220 fluids spiked with varying concentrations of propranolol ranging from 0 to 120 muM, and clear trends
221 of 88% of patients who received the selected propranolol regimen showed improvement by week 5, versus
222 y assigned to receive placebo or one of four propranolol regimens (1 or 3 mg of propranolol base per
223 nterestingly, intra-BLA, but not intra-mPFC, propranolol rescued the IED; animals receiving intra-BLA
224 hat systemic beta-adrenoceptor blockade with propranolol rescues the IED, but impairs delayed extinct
225 9.9-fold for 1 microM CGP 12177 and 1 microM propranolol, respectively) and abolished in beta1-adreno
230 of stressed animals with the beta-antagonist propranolol reversed the stress-induced macrophage infil
231 the beta-noradrenergic receptor antagonist, propranolol, reversed the decrease, suggesting that the
233 removed from water, while the organic cation propranolol showed biouptake similar to that of TCC.
238 revealed that noradrenergic blockade (40 mg propranolol) significantly increased metacognitive perfo
240 cacy and safety of a pediatric-specific oral propranolol solution in infants 1 to 5 months of age wit
241 ction and quantification of the beta-blocker propranolol spiked into human serum, plasma, and urine a
242 In this hypermetabolic, hypoglycaemic state, propranolol stimulated a rise in P aC O2, suggestive of
243 gy state were inhibited by coincubation with propranolol, suggesting involvement of beta-adrenergic s
245 sence of AGP was found to be greater for (S)-propranolol than (R)-propranolol for solutions containin
246 nt from baseline to 2 hours was greater with propranolol than placebo (median, -4.5 versus 0 arbitrar
248 tenuated by the beta-adrenoceptor antagonist propranolol, the mixed alpha-/beta-adrenoceptor antagoni
252 Simultaneous administration of atropine and propranolol to block parasympathetic and sympathetic bra
253 Control animals treated with intravenous propranolol to block sympathetically mediated chronotrop
255 a(V)1.1 channels in vivo, and treatment with propranolol to inhibit beta-adrenergic receptors reduced
263 e of incomplete development, the efficacy of propranolol treatment in retinopathy needs to be evaluat
264 cal trials are currently ongoing to evaluate propranolol treatment in stage 2 ROP patients who tend t
266 less future recovery of responding, whereas propranolol treatment reduced the benefit seen with comp
267 d norepinephrine levels in the pancreas, and propranolol treatment reversed glucose intolerance in th
271 e of the treatment approaches at any dose of propranolol (up to 60 mg/kg/day) were effective in preve
275 tamine challenge was partially attenuated by propranolol versus placebo: FEV1% mean difference, 5.28
276 ea under the naphthalene ring vibration from propranolol was 133.1 ng/mL (0.45 muM), 156.8 ng/mL (0.5
279 ric detection of the protonated beta-blocker propranolol was explored at arrays of nanoscale interfac
283 al of 10% of patients in whom treatment with propranolol was successful required systemic retreatment
284 aximum length of treatment was 4 months, and propranolol was suspended when complete regression of le
285 ent events differed by drug (p = 0.004), and propranolol was the least effective compared with the ot
286 mination of the enantiomers of a basic drug, propranolol, was achieved at a micro liquid-liquid inter
288 Patients with refractory ascites taking propranolol were found to have poorer outcomes than thos
289 udy, patients with refractory ascites taking propranolol were found to have poorer outcomes, perhaps
290 sing scan rate, useful whole-body images for propranolol were obtained from the tissues even at 7 mm/
291 During summer, atenolol, metoprolol, and propranolol were rapidly attenuated in the pilot-scale s
294 formation rates increased for metoprolol and propranolol when algal photosynthesis was supported by i
296 n through co-treatment with the beta-blocker propranolol, while leaving the peripheral effect intact,
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