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1 on of a shortacting beta(2) agonist (180 mug salbutamol).
2 nse to an endothelium-dependent vasodilator (salbutamol).
3 ss (p<0.001), in the group receiving regular salbutamol.
4  The change in VMAX was partially blocked by salbutamol.
5                These changes were blocked by salbutamol.
6 chronic stimulation was partially blocked by salbutamol.
7 on to ICS and the short-acting beta2-agonist salbutamol.
8 ng treatment with salmeterol, formoterol, or salbutamol.
9 mine and norepinephrine but not with that of salbutamol.
10  or combined with 3,4-diaminopyridine and/or salbutamol.
11 ation can be measured by FMD and by PWA with salbutamol.
12 turally related non-catechol partial agonist salbutamol.
13  by 59 +/- 7% (n = 5) and inhibited those to salbutamol (0.3 to 3.5 nmol.min-1) by 52 +/- 6% (n = 8).
14                          Cumulative doses of salbutamol (0.3 to 3.5 nmol.min-1) did not cause tachyph
15                                              Salbutamol (1-10 microM) inhibited iKCa1 currents follow
16 AR stimulation with epinephrine 10(-6) M and salbutamol 10(-6)-10(-5) M yielded a strong cyclic adeno
17 ombination MDI with one to two actuations of salbutamol (100 mug per actuation) by MDI as needed for
18 (69-201 ppb) and to control eyes spiked with salbutamol (100 ppb) and terbutaline (25-100 ppb).
19 ere randomized to treatment with intravenous salbutamol (15 microg kg(-1) h(-1)) or placebo for 7 d.
20 set were randomly assigned to receive either salbutamol (15 mug/kg ideal bodyweight per h) or placebo
21  65 of 69 patients who received ephedrine or salbutamol, 18 of 29 who were given 3,4-diaminopyridine,
22                                              Salbutamol (2.5 mg) was administered by inhalation.
23 e samples (91) from athletes with detectable salbutamol (30) and negative samples (61) were analyzed
24 ctivation of beta2 adrenergic receptors with salbutamol (40 microm) or formoterol (5 microm) resulted
25  was no evidence that regular use of inhaled salbutamol 400 microg four times daily for a year increa
26 efore inhalation of a bronchodilating agent (salbutamol 400 mug), and one set was acquired after.
27     HI reversibility after administration of salbutamol (400 mug) was defined as a decrease in RV >20
28                                              Salbutamol, a beta 2-agonist, increased the weight of th
29                                         (iv) Salbutamol, a beta-AR partial agonist, acutely decreased
30 in 4 million Norwegians, the beta2AR agonist salbutamol, a brain-penetrant asthma medication, was ass
31 nd engage the rotamer toggle switch, whereas salbutamol, a noncatechol partial agonist only breaks th
32  agonist, norepinephrine; a partial agonist, salbutamol; a weak partial agonist, dopamine; a very wea
33 = 1.5) or 'extreme' salbutamol overuse (> 32 salbutamol actuations/24-h period).
34  and purine metabolism have association with salbutamol administration.
35                               Formoterol and salbutamol also showed anti-inflammatory properties.
36 osure to beta2-adrenoceptor agonists such as salbutamol, an effect postulated to operate via intracel
37 ol and isoprenaline and the partial agonists salbutamol and dobutamine.
38                                   The use of salbutamol and ephedrine alone or combined with pyridost
39 ntake of small amounts of the model compound salbutamol and explore a sensitive approach to help scre
40 andomly allocated (1:1) to receive nebulised salbutamol and ipratropium bromide with either 2.5 mL of
41 essment, including responsiveness to inhaled salbutamol and ipratropium bromide.
42  that the release was partially inhibited by salbutamol and salmeterol.
43 a short-acting beta(2)-adrenoceptor agonist (salbutamol) and a short-acting anticholinergic (ipratrop
44                                   Albuterol (salbutamol) and glyceryl trinitrate (GTN) were administe
45 cAMP production in response to short-acting (salbutamol) and long-acting (formoterol) beta2 -agonists
46                  Our results using atenolol, salbutamol, and cocaine as test compounds show that we c
47  most beta2-AR agonists, including zinterol, salbutamol, and procaterol, was potentiated by PTX, indi
48 ngly, the beta-adrenergic receptor agonists, salbutamol, arterenol and isoproterenol were also able t
49 stemic corticosteroid for 3 days and inhaled salbutamol as long as they needed.
50 mation for clinicians considering metrics of salbutamol as predictors of future adverse outcomes in a
51 gimen (SMART) with a fixed-dose regimen with salbutamol as reliever ('Standard'), actual medication u
52 pranolol (non-selective beta-antagonist) and salbutamol (beta(2)-agonist), which are known to alter t
53 1; mean +/- SD) but only weak relaxations to salbutamol (beta(2)-receptor agonist; 13 +/- 3%; P < 0.0
54 pproaches, we show that the aromatic ring of salbutamol binds to a different site on the beta(2)AR th
55               Simultaneous administration of salbutamol blocked these changes in protein expression a
56                                 Anti-TNF and salbutamol both suppressed clinical arthritis more effec
57 easurements of vascular responses to inhaled salbutamol by pulse wave analysis (PWA) or pulse contour
58 fate to SABA, and levosalbutamol compared to salbutamol cannot be recommended in routine practice.
59            It is of particular interest that salbutamol changed the relative levels of SERCA proteins
60                  In this study, we show that salbutamol closes iKCa1 in mast cells derived from human
61                                              Salbutamol decreased the levels of the slow-twitch cardi
62                                              Salbutamol did not change the level of myosin heavy chai
63                                              Salbutamol did not produce these effects in the vastus i
64 periments indicate that the aromatic ring of salbutamol does not activate this mechanism either direc
65                   Treatment with intravenous salbutamol early in the course of ARDS was poorly tolera
66                               Salmeterol and salbutamol enhanced rhinovirus- and IL-1beta-induced IL-
67 ular coherence and tremor, and the fact that salbutamol enhances tremor but does not affect coherence
68                                  Intravenous salbutamol failed to reduce Rp as effectively in challen
69 olled phase 2 trial, intravenous infusion of salbutamol for up to 7 days in patients with acute respi
70 nity or selectivity of other beta2-agonists (salbutamol, formoterol, fenoterol, clenbuterol, or adren
71 wer Murray lung injury score at Day 7 in the salbutamol group (1.7 +/- 0.9) versus placebo (2.0 +/- 0
72 au airway pressure was lower at Day 7 in the salbutamol group (23.9 +/- 3.8 cm H2O) versus placebo (2
73     We randomly assigned 162 patients to the salbutamol group and 164 to the placebo group.
74                              Patients in the salbutamol group had a higher incidence of supraventricu
75                              Patients in the salbutamol group had significantly lower lung water at D
76 tality (55 [34%] of 161 patients died in the salbutamol group vs 38 (23%) of 163 in the placebo group
77         An enantioselective synthesis of (R)-salbutamol has been carried out using the chiral, C2 sym
78 nfirm the efficacy and safety of intravenous salbutamol in ALI/ARDS, this trial provides the first pr
79  group or more than 16 actuations per day of salbutamol in the standard group).
80                                              Salbutamol increased 28-day mortality (55 [34%] of 161 p
81       The uphill step in the partial agonist salbutamol induced activation is distinct from full agon
82 -9.68 +/- 0.07, n = 17, for isoprenaline and salbutamol-induced responses, respectively).
83 ed in 68 asthmatic patients before and after salbutamol inhalation.
84 ly and group B (40 patients) received rescue salbutamol inhalation.
85 2%]; adjusted HR, 1.22 [95% CI, 1.11-1.34]), salbutamol inhaler prescription at age 5 years (10.34% v
86 risk of asthma requiring hospital admission, salbutamol inhaler prescription at age 5 years, and all-
87  hospital admission; secondary outcomes were salbutamol inhaler prescription at age 5 years, obesity
88 risk of asthma requiring hospital admission, salbutamol inhaler prescription at age 5 years, obesity
89    A third group (30) was created by spiking salbutamol into negative samples to eliminate confoundin
90 3, TM5, and TM6, whereas the binding site of salbutamol is shifted toward TM4.
91 This analysis suggests that (1) ephedrine or salbutamol is the first choice of treatment in DOK7 CMS;
92 of agonist norepinephrine or partial agonist salbutamol leads to the selection of a subset of conform
93     Instead, we suggest that propranolol and salbutamol may affect both tremor and corticomuscular co
94 e beta2 adrenoceptor agonists formoterol and salbutamol mediated suppression of IL-27p28 production,
95 opionate and beta(2) agonists salmeterol and salbutamol on IL-6 production in BEAS-2B and primary bro
96 pplication of chronic muscle stimulation and salbutamol on the expression of mRNAs and proteins norma
97  opener 1-EBIO, and was reversed by removing salbutamol or by the addition of the selective beta2-adr
98 tients were randomised to receive 400 microg salbutamol or matched placebo via a Diskhaler four times
99 nce of isoprenaline and adrenaline than when salbutamol or terbutaline were present (e.g., log KD pro
100  antiinterleukin-12 (anti-IL-12) antibodies, salbutamol, or indomethacin.
101 in 1 h) alongside standard therapy including salbutamol, or placebo control plus standard therapy alo
102  asthma control (ACQ-5 >/= 1.5) or 'extreme' salbutamol overuse (> 32 salbutamol actuations/24-h peri
103 ted with an increased risk of future extreme salbutamol overuse.
104 re identified as hypoxanthine increased with salbutamol (p < 0.001).
105 w-mediated dilation (p < 0.001) and PWA with salbutamol (p = 0.03) responses fell after typhoid vacci
106 o select features correlated with detectable salbutamol (p(corr) > 0.5) and ROC analysis was performe
107 si muscle and simultaneous administration of salbutamol partially blocked this change.
108 2 signaling complex, beta(2)-AR stimulation (salbutamol plus atenolol) of I(Ca,L) was examined in per
109 a dynamic harmonic regression (DHR) model to salbutamol prescribing in relation to temperature.
110 eral well-known beta2-adrenoceptor agonists (salbutamol, procaterol, and fenoterol).
111                             Correlation with salbutamol (r = 0.415, p < 0.01, Spearman's correlation)
112                                 Furthermore, salbutamol recovery post-challenge was significantly blu
113                                              Salbutamol responses were more variable with PWA (adults
114 nitude of treatment effect with ephedrine or salbutamol seems to increase gradually, peaking after ap
115                                       Whilst salbutamol significantly increased tremor amplitude as e
116            Virtual ligand screening with the salbutamol-stabilized conformation shows enrichment of n
117 stamine infusions, volume resuscitation, and salbutamol sulfate inhalation, which resulted in an impr
118 imulations with the G protein-biased agonist salbutamol that involves perturbations of the network of
119  study the effects of regular use of inhaled salbutamol, the most widely prescribed bronchodilator in
120  0.30 mug/min and 0.60 mug/min intracoronary salbutamol) to measure changes in segmental lumen volume
121  observed in homogenates of muscles from the salbutamol-treated animals and could partially account f
122         The aim of TRUST (The Regular Use of Salbutamol Trial) was to study the effects of regular us
123 eported (day- and nighttime asthma symptoms, salbutamol usage, and 7-item-Asthma Control Questionnair
124 ) (95% CI) 1.24 (1.06-1.46)], higher days of salbutamol use (per 2 days in 2 weeks) [OR 1.15 (1.00-1.
125                            Higher mean daily salbutamol use (per two actuations/day) [Odds ratio (OR)
126                            Higher mean daily salbutamol use [OR 2.73 (1.84-4.07)], number of days of
127 e relationships between different metrics of salbutamol use and future risk are uncertain.
128 Electronically recorded frequency of current salbutamol use is a strong predictor of risk of future a
129 the relationship between metrics of baseline salbutamol use over 2 weeks and future severe asthma exa
130                            Higher mean daily salbutamol use was associated with future poor asthma co
131                        Bronchodilation after salbutamol was equal to or greater than that after iprat
132                                              Salbutamol was more than 100 times as potent as dobutami
133                          Odds of exposure to salbutamol were similar.

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