Disease relevance of Aeromax

• Effect of long-term salmeterol treatment on exercise-induced asthma [1].
• Combined salmeterol and fluticasone in the treatment of chronic obstructive pulmonary disease: a randomised controlled trial [2].
• There were no significant pretreatment differences between the salmeterol and control groups in the severity of symptoms or the degree of airway obstruction [3].
• Effect of salmeterol on Pseudomonas aeruginosa infection of respiratory mucosa [4].
• Salmeterol inhibits inflammatory responses by neutrophils and mononuclear cells in vitro and in mouse models of lung inflammation in vivo [5].

Psychiatry related information on Aeromax

• In addition, the mean time to first exacerbation in the combination therapy group was significantly longer compared with that of the salmeterol group (128 vs. 93 d, p < 0.0001) [6].
• We assessed the patient-perceived effect of treatment with fluticasone propionate/salmeterol combination (FSC), compared with fluticasone propionate (FP) or salmeterol (SAL) alone, on activity limitations, particularly strenuous physical activities [7].
• The area under the 12-h time-response curve for FEV1 was greater for both formulations of salmeterol (MDI and DPI) than for albuterol [8].
• When compared with current treatment for chronic obstructive pulmonary disease, tiotropium is at least as effective as salmeterol and more effective than ipratropium; moreover, the once-a-day dosing increases the likelihood of patient compliance [9].

High impact information on Aeromax

• The morning dose of salmeterol attenuated the degree of bronchoconstriction at all times (decrease in FEV1 on day 1, 5+/-2 percent; on day 14, 10+/-3 percent; and on day 29, 9+/-3 percent; P=0.10) [1].
• The role of long-acting beta2-adrenergic-receptor agonists, such as salmeterol, needs to be defined [10].
• We compared a new long-acting, inhaled beta 2-adrenoceptor agonist, salmeterol, with a short-acting beta 2-agonist, albuterol, in the treatment of mild-to-moderate asthma [11].
• There was a significant increase in FEV1 one hour after the inhalation of salmeterol (P = 0.006), which did not differ significantly on days 0, 28, and 56 of the treatment period (increase, 9.8, 9.4, and 8.8 percent of predicted FEV1, respectively; P = 0.91) [12].
• We investigated the long-term effects of the beta 2 agonist salmeterol on bronchodilation and on airway hyperresponsiveness to the bronchoconstrictive agent methacholine in mild asthma [12].

Chemical compound and disease context of Aeromax

• We evaluated the preventive effect on exercise-induced bronchospasm (EIB) of a single 42 micrograms dose of salmeterol, a uniquely long-acting inhaled bronchodilator, and compared salmeterol with 180 micrograms albuterol in two independent, randomized, double-blind, placebo-controlled studies involving 161 subjects [13].
• We studied the duration of the bronchodilation and the protective effect against methacholine-induced airway obstruction of a single dose of salmeterol in a double-blind, randomized, placebo-controlled, crossover design [14].
• Comparison of duration of agonist action at beta 1- and beta 2- adrenoceptors in C6 glioma cells: evidence that the long duration of action of salmeterol is specific to the beta 2-adrenoceptor [15].
• Long-acting beta2 agonist bronchodilators (e.g. formoterol, salmeterol) are a new interesting therapeutic option for patients with chronic obstructive pulmonary disease (COPD) [16].
• In patients with chronic obstructive pulmonary disease (COPD), tiotropium 18microg once daily significantly improved lung function compared with placebo and ipratropium 40microg four times daily in 1-year trials or salmeterol 50microg twice daily in a 6-month study [17].

Biological context of Aeromax

• Salmeterol remained effective in terms of disease control, with a significant improvement in morning PEFR compared with placebo that was maintained over the 4 week treatment period.(ABSTRACT TRUNCATED AT 250 WORDS)[18]
• After a 2 week run-in without beta-2 agonists, 17 asthmatic patients (mean [SE] age 34 [3] years, mean forced expiratory volume in 1 s [FEV1] 64 [2.7]% of predicted) were randomised to receive salmeterol 50 micrograms twice daily or placebo for 4 weeks in a double-blind cross-over fashion [18].
• In this respect, there is strong evidence for the existence of specific additional binding sites (exosites) for salmeterol and related compounds, and that exosites exist on non-ligand recognition regions of the beta 2-adrenoceptor protein [19].
• Additionally, salmeterol did not affect the maximal heart rate achieved during the test as compared with the placebo [20].
• RESULTS: There was sustained and significant improvement (P < .001) over baseline in all measures of asthma control in subjects receiving salmeterol, regardless of Arg16Gly genotype [21].

Anatomical context of Aeromax

• There was a significant reduction in lymphocyte beta-2 adrenoceptor density after salmeterol compared with placebo and run-in [18].
• Here, we describe the ligand-independent activation of GR by the beta2-adrenergic receptor (beta2-AR) agonists, salbutamol and salmeterol, in primary human lung fibroblasts and vascular smooth muscle cells [22].
• In the week before clinical exacerbation, sputum eosinophil counts were higher in the salmeterol-treatment arm (19.9 +/- 29.8% [mean +/- SD], versus placebo 9.3 +/- 17.6%; p = 0.006) [23].
• Thus, in contrast to albuterol, salmeterol did not demonstrate mast-cell stabilizing properties in vivo at a time corresponding to maximal bronchodilatation [24].
• Effects of salmeterol on smooth muscle versus inflammatory outcomes [25].

Associations of Aeromax with other chemical compounds

• Treatment failure occurred in 46.3% (95% CI, 34%-59%) of the salmeterol-minus group 8 weeks after triamcinolone therapy was eliminated compared with 13.7% (95% CI, 5%-22%) of the salmeterol-plus group [26].
• Combined salmeterol and fluticasone for COPD [27].
• Oral montelukast versus inhaled salmeterol to prevent exercise-induced bronchoconstriction [28].
• The protective effects by increasing cumulative doses of formoterol (12, 60, 120 micrograms) and salmeterol (50, 250, 500 micrograms) on methacholine-induced bronchoconstriction were evaluated in a double-blind, crossover, placebo-controlled design [29].
• CONCLUSION: The meta-analysis indicates that the fluticasone propionate plus salmeterol combination offers the potential for increased clinical efficacy over concurrent use of the same doses of the same 2 drugs [30].

Gene context of Aeromax

• Analyses of anti-EBP50 protein immunoprecipitate showed that salmeterol induced an increase in the amount of CFTR that binds to EBP50 [31].
• Eotaxin inhibition was transcriptional and additively enhanced by the glucocorticoid fluticasone and the beta(2)-agonist salmeterol, whereas MCP-1 inhibition was post-transcriptional and additively and synergistically enhanced by fluticasone and salmeterol, respectively [32].
• However, after 20 to 30 min of treatment, agonists with intermediate strengths, such as albuterol and salmeterol, stimulate GRK site phosphorylations that are approximately equal to that produced by epinephrine, and the correlation breaks down [33].
• In addition, salmeterol in combination with FP enhanced glucocorticoid response element (GRE)-luciferase reporter gene activity and mitogen-activated protein kinase phosphatase 1 (MKP-1) and secretory leuko-proteinase inhibitor (SLPI) gene induction [34].
• Here, we tested the effects of the beta(2)-agonists salbutamol (Salbu) and salmeterol (Salme) on IL-8 release and tumor necrosis factor (TNF)-alpha-induced IL-8 release from ASM cells [35].

Analytical, diagnostic and therapeutic context of Aeromax

• In a parallel, double-blind study, 24 patients with mild asthma were randomly assigned to treatment with either inhaled salmeterol (50 micrograms, twice daily) (n = 12) or placebo (n = 12) during an eight-week trial [12].
• MAIN OUTCOME MEASURE: Time to asthma treatment failure in patients receiving salmeterol [26].
• The other half of the salmeterol group (salmeterol-plus group) was randomly assigned to continue both salmeterol and triamcinolone for the remaining 16 weeks (active control group) [26].
• We found that TNF-alpha stimulated eotaxin release (assayed by ELISA) from HASM cells and that the release was partially inhibited by salbutamol and salmeterol [36].
• We conducted a double-blind, placebo-controlled, crossover study of the effect of the long-acting beta(2)-agonist salmeterol on airway inflammation induced by segmental allergen challenge (SAC) [37].

References