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1 eatment with a bronchodilator (180 microg of albuterol).
2 as-needed ICS treatment coadministered with albuterol.
3 er nasal suctioning and a trial of nebulized albuterol.
4 with COPD, including those "unresponsive" to albuterol.
5 /ml) and they lost the Qaw responsiveness to albuterol.
6 S)-enantiomer after long-term use of racemic albuterol.
7 d) was initiated 3 h before and 0.25 h after albuterol.
8 ing to viscoelastic tissues before and after albuterol.
9 ol, and -3.45 +/- 0.92 mm Hg at 20 min after albuterol.
10 after administration of both salmeterol and albuterol.
11 n tolerance to the bronchodilator effects of albuterol.
12 ing disorders before and after inhalation of albuterol.
13 ilar in both groups and did not change after albuterol.
14 scribed racemic albuterol is composed of (S)-albuterol.
15 oride and after reversal of provocation with albuterol.
16 the beta2AR-27 polymorphism and response to albuterol.
17 ht) was given orally with the second dose of albuterol.
18 EX, then challenged with media or 100 microM albuterol.
19 not changed by TNF-alpha or by any isomer of albuterol.
20 favorably to ephedrine, pseudoephedrine, or albuterol.
21 atients with COPD who received four puffs of albuterol.
22 and fenoterol and 100 times more potent than albuterol.
23 se dependent manner, but not by (S) or (R,S)-albuterol.
24 uction scores were lower for sheep receiving albuterol.
25 0 minutes after inhalation of 180 micro g of albuterol.
26 e) and 200 microg metered-dose inhaler (MDI) albuterol.
27 ephedrine, 0.250 with dobutamine, 0.148 with albuterol, 0.194 with fenoterol, and 0.212 with epinephr
30 luid clearance was increased by both racemic albuterol 10(-6) M (14.5 +/- 3.0%, p <.05) and R-enantio
33 as also compared with unlabeled monodisperse albuterol (15-microg dose) and 200 microg metered-dose i
34 onsisted of baseline FEV1, pretreatment with albuterol 180 micrograms, postbronchodilator spirometry
38 he children received a nebulized solution of albuterol (2.5 or 5 mg per dose, depending on body weigh
39 rine (100%) were 42% for fenoterol, 4.9% for albuterol, 2.5% for dobutamine, and 1.1% for ephedrine.
41 volume pulse during intravenous infusion of albuterol (5 microg/min, DeltaRI(ALB)) and glyceryl trin
45 acid (3), riluzole (6), hydroxyurea (7), and albuterol (9), none of which has demonstrated clinical e
49 termined the response to increasing doses of albuterol administered by a MDI and cylindrical spacer t
55 inhaled technetium-99m-labeled monodisperse albuterol aerosols (30-microg dose) of 1.5-, 3-, and 6-m
58 ent asthma should not be treated with rescue albuterol alone and the most effective treatment to prev
60 e and homogeneous changes in spirometry with albuterol, along with greater changes in these measures
61 to tiotropium include a positive response to albuterol and airway obstruction, factors that could hel
63 e observed beginning with the lowest dose of albuterol and continuing throughout the dose-response as
64 thma, the addition of ipratropium bromide to albuterol and corticosteroid therapy significantly decre
65 IP(DVP), whereas systemic administration of albuterol and GTN produced dose-dependent reductions in
66 gonists with intermediate strengths, such as albuterol and salmeterol, stimulate GRK site phosphoryla
67 on gas exchange of salmeterol with those of albuterol and the anticholinergic agent ipratropium in 2
68 re and after administration of 180 microg of albuterol, and a positive response was considered an inc
69 re and up to 4 h after inhalation of racemic albuterol, and determined the unchanged R/S ratio in uri
72 assess lower respiratory tract deposition of albuterol, and show that MDIs are more efficient for aer
73 e presence of the short-acting beta2-agonist albuterol, and the long-acting beta2-agonists formoterol
75 aily beclomethasone with beclomethasone plus albuterol as rescue (combined group); twice daily beclom
76 twice daily beclomethasone with placebo plus albuterol as rescue (daily beclomethasone group); twice
78 twice daily placebo with beclomethasone plus albuterol as rescue (rescue beclomethasone group); and t
80 ured plasma levels of unchanged (R)- and (S)-albuterol before and up to 4 h after inhalation of racem
81 ects derived from the regular use of inhaled albuterol beyond those derived from use of the drug as n
82 at Met772-AC9 is associated with an improved albuterol bronchodilator response in asthmatics was inve
83 cohort of 203 527 patients who began taking albuterol but did not receive antipsychotic medication.
86 5) decreases in Raw and tissue damping after albuterol, but tissue elastance decreased only in the Ty
87 response to regular versus as-needed use of albuterol by genotyping the 190 asthmatics who had parti
88 n minutes after administration of 180 microg albuterol by metered dose inhaler, mean Qaw increased by
89 m bromide with the second and third doses of albuterol; children in the control group received 2.5 ml
90 FR during treatment with regularly scheduled albuterol compared with placebo (14 L/min [95% CI 3 to 2
93 ontinuous nebulization group, or d) 40 mg of albuterol continuous nebulization group (n=5 animals per
94 e continuous nebulization group, c) 20 mg of albuterol continuous nebulization group, or d) 40 mg of
97 bo-controlled trials have shown that inhaled albuterol decreases the duration of cough in adults with
98 used to determine significant differences in albuterol delivered or lost among the operating frequenc
101 ined the effect of various He-O2 mixtures on albuterol delivery from metered-dose inhalers (MDIs) and
102 idity, and spontaneous respiratory effort on albuterol delivery in a model of the trachea and bronchi
106 the nebulizer was operated with O2, greater albuterol delivery was achieved when the ventilator circ
108 ions and with a frequency of 10 breaths/min, albuterol delivery with CMV (VT, 800 ml; 30.3 +/- 3.4%),
110 greater bronchodilation than 200 microg MDI albuterol (deltaFEV1 [ml]: 6 microm [551], 3 microm [457
113 demonstrates that, in emergency situations, albuterol does not relieve acute airway obstruction in a
116 statistically significant differences in the albuterol dose response following salmeterol or placebo.
118 gned 255 patients with mild asthma to inhale albuterol either on a regular schedule (126 patients) or
120 d in the circuit's expiratory limb collected albuterol exiting the endotracheal tube and any albutero
121 ling efficiency, with ephedrine, dobutamine, albuterol, fenoterol, and epinephrine giving 0, 7, 17, 4
122 ditional inhaled short-acting beta2-agonists albuterol, fenoterol, and terbutaline provide rapid as-n
123 corticosteroids, post 180 microg aerosolized albuterol, FEV(1) was 74 +/- 23% predicted and FEV(1)/FV
125 (S)-albuterol (the inactive isomer) or (R,S)-albuterol for 90 minutes before adding 2 ng/ml TNF-alpha
127 Compared with saline and control groups, the albuterol groups had lower pause and peak inspiratory pr
129 terol = fenoterol > terbutaline = zinterol = albuterol > salmeterol > dobutamine > or = ephedrine.
130 d on the basis of bronchodilator response to albuterol (> 12% and > 200-ml improvement) and were rand
131 tudy Arg Arg patients who had regularly used albuterol had a morning peak expiratory flow 30.5 +/- 12
134 day when compared with placebo, suggest that albuterol improves pulmonary function in a majority of h
136 w (Qaw) and FEV (1) before and after inhaled albuterol in 19 glucocorticosteroid (GS)-naive patients
137 xpression was significantly inhibited by (R)-albuterol in a dose dependent manner, but not by (S) or
138 ncrease in Qaw and its hyporesponsiveness to albuterol in asthmatic subjects may be consequences of a
140 tes to individual differences in response to albuterol in Latinos, notably in SLC genes that include
141 no decline in peak flow with regular use of albuterol in patients who were homozygous for glycine at
143 Currently we have completed a pilot study of albuterol in patients with late-onset Pompe disease alre
144 thma severity and bronchodilator response to albuterol in Puerto Ricans and Mexicans with asthma.
148 ) was significantly (p < 0.01) reduced after albuterol inhalation (60.6 +/- 22.2 cm H(2)O/L/s) but pr
149 rolled, randomized crossover trial comparing albuterol inhalation aerosol with a saline placebo.
154 vention did not differ significantly for the albuterol inhaler (50% improvement), placebo inhaler (45
156 ents with asthma to active treatment with an albuterol inhaler, a placebo inhaler, sham acupuncture,
159 n dyspnea in patients with COPD with inhaled albuterol is in part due to increased diaphragmatic cont
160 treatment of ASM cultures with beta-agonists albuterol, isoproterenol, or salmeterol (100 nM to 10 mu
162 etered-dose inhaler (MDI), we measured serum albuterol levels after administration by a MDI and space
167 a Ca2+ agonist in airway smooth muscle, (S)-albuterol may have profound clinical implications becaus
168 to week 48 in mean daily number of puffs of albuterol, mean total asthma symptom score, and mean ove
171 ed corticosteroids as rescue medication with albuterol might be an effective step-down strategy for c
172 d at baseline and 10 min after inhalation of albuterol (n = 28) or placebo (n = 13) using a metered-d
174 had a significantly higher heart rate after albuterol nebulization compared with the control group.
176 lude that during acute asthma exacerbations, albuterol nebulized with heliox leads to a more signific
177 rty-five patients were randomized to receive albuterol nebulized with oxygen (control) versus heliox
179 second, the number of puffs of supplemental albuterol needed, asthma symptoms, asthma quality-of-lif
180 ts had reversibility in FEV1 after nebulized albuterol of 15% or more and a mean postbronchodilator F
183 onsiveness, we determined the effects of (S)-albuterol on intracellular Ca2+ concentration ([Ca2+]i)
185 L IMPLICATION: The suppressive effect of (R)-albuterol on neural ICAM-1 expression may be an addition
186 atients randomly received inhaled placebo or albuterol on the first test day and the alternative medi
196 to a short-acting bronchodilator, especially albuterol, predicted a positive clinical response to tio
200 proved FEV(1) in these patients with asthma, albuterol provided no incremental benefit with respect t
202 oint [CI, 0.15 to 0.43]), reduced mean daily albuterol puffs (-0.27 puff/d [CI, -0.49 to -0.04 puff/d
204 so declined in the Arg/Arg patients who used albuterol regularly but not in those who used albuterol
208 and 86.8%, respectively; P=0.50), use of an albuterol rescue inhaler (2.8 and 3.0 inhalations per we
209 scores (0.2 units, p = 0.034), and increased albuterol rescue use (0.95 puffs/d, p = 0.004) compared
212 d clinical features, airflow limitation, and albuterol responsiveness in adults acutely ill with asth
213 nsistent with this AC9 polymorphism altering albuterol responsiveness in the context of concomitant i
215 ong the 39 patients who completed the study, albuterol resulted in a 20% increase in FEV(1), as compa
219 ich all patients returned to using as-needed albuterol, so that by the end of the study Arg Arg patie
220 ressing Met772 had a significantly increased albuterol-stimulated adenylyl cyclase response (approxim
221 wer after treatment with the partial agonist albuterol, suggesting a correlation between the efficien
222 ator to produce (99m)Tc-labeled monodisperse albuterol sulfate aerosols of 1.5-, 3-, and 6- micro m m
224 examined included the antiasthma medication albuterol sulfate and the antiobesity medications orlist
228 had lower morning PEFR during treatment with albuterol than during the placebo period, when albuterol
230 ither (R)-albuterol (the active isomer), (S)-albuterol (the inactive isomer) or (R,S)-albuterol for 9
231 ral or intravenous administration of racemic albuterol, the (R)- enantiomer is metabolized several ti
232 itude but was more prolonged than that after albuterol, the greatest mean change being -2.74 +/- 0.89
234 fficacy in an open label study of adjunctive albuterol therapy in patients with late-onset Pompe dise
237 Spiros actuation delivers 1.12 times as much albuterol to the airways as one Ventolin actuation (90%
242 ll subjects responded promptly to additional albuterol treatment, and no subject developed refractory
246 ores (-1.0 +/- 0.1 vs. -0.6 +/- 0.1), rescue albuterol use (-3.3 +/- 0.2 vs. -1.9 +/- 0.2 puffs/d), a
247 with moderate-to-severe asthma with frequent albuterol use and nighttime awakenings at least once wee
248 s the characterization of effects of regular albuterol use in patients with genetic variations in the
251 buterol than during the placebo period, when albuterol use was limited (-10 L/min [-19 to -2]; p=0.02
253 re function had more asthma symptoms, rescue albuterol use, and FEV(1) reversal (P < 0.001, 0.03, and
254 FEV1, peak expiratory flow, symptoms, rescue albuterol use, and quality of life scores, also did not
255 duced asthma symptom scores and supplemental albuterol use, and significantly increased the percentag
256 mptoms and albuterol use, night symptoms and albuterol use, controller treatment, lung function measu
257 I scores include 5 domains: day symptoms and albuterol use, night symptoms and albuterol use, control
260 duled use of inhaled albuterol with those of albuterol used only as needed in patients with mild chro
261 responsiveness to the inhaled beta-agonist, albuterol, using changes in maximal expiratory flows.
262 s were used to administer 2000 micrograms of albuterol, using either a collapsible or a rigid spacer.
263 at 7:00 A.M. was 10.7, 14.8, and 19.6% with albuterol versus 2.4, 1.0, and -0.8% with placebo (p = 0
264 .M. pretherapy) was 8.1, 10.1, and 9.7% with albuterol versus 3.9, 3.5 and 2.6% with placebo (p = 0.0
265 ificantly more positive and homogeneous with albuterol versus placebo at both 7:00 A.M. and 3:00 P.M.
266 was significantly greater (p < 0.05) in the albuterol versus placebo group for FEV(0.5) (2.2% versus
267 han 8% change in FEV1 separated changes with albuterol versus placebo with 96% specificity and occurr
269 ease in airway resistance with four puffs of albuterol was comparable to that observed with cumulativ
272 sus baseline), and the Qaw responsiveness to albuterol was restored ( +21 +/- 2%; p < 0.05) in the as
274 1 after cumulative doubling doses of inhaled albuterol were assessed after a 2-wk beta-agonist washou
275 e validation data showed that technetium and albuterol were coassociated on each impactor stage for a
279 In contrast, bronchodilator responses to albuterol were similar in eosinophilic and noneosinophil
280 hort-term bronchodilator response to inhaled albuterol were small and judged to be clinically unimpor
281 centage change in FEV(1) after 180 microg of albuterol, were adjusted to account for sex, age, height
282 The EPR was blocked by cromoglycate and albuterol, whereas the LPR was abolished by cromoglycate
285 rdingly, 10 healthy subjects inhaled racemic albuterol with a MDI alone and with a MDI and holding ch
286 nantiomer disposition after inhaling racemic albuterol with a metered-dose inhaler (MDI) is not known
288 ffects of regularly scheduled use of inhaled albuterol with those of albuterol used only as needed in
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