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PubMed2001

Exhaled nitric oxide decreases during exercise-induced bronchoconstriction in children with asthma.

Nitric oxide (NO) produced in the airways can be either detrimental or protective to the host. To investigate the role of NO in the pathogenesis of exercise-induced bronchoconstriction (EIB), we measured exhaled NO (ENO) after exercise challenge in 39 asthmatic and six normal children. FEV(1) and ENO were measured before and at 0, 5, 10, and 15 min after exercise performed on a treadmill for 6 min. EIB was defined as a decrease in FEV(1) of more than 15% after the exercise. Normal children (control group) did not have EIB. Twenty-one patients with asthma had EIB (EIB group) whereas the remaining 18 patients did not (non-EIB group). The baseline ENO value was significantly higher in the asthmatic children than in the normal children, and there was a positive correlation between the maximal percent decrease in FEV(1) and the baseline ENO value (r = 0.501, p = 0.012). At the end of the exercise, ENO had decreased in all the subjects. In the non-EIB and control groups, ENO rebounded to above the baseline at 5 min after the exercise and thereafter. In contrast, ENO remained at a decreased level in the EIB group. The change in ENO did not correlate with the change in minute ventilation, and beta-agonist inhalation at the peak of EIB that accelerated the recovery of FEV(1) did not affect the depressed level of ENO, demonstrating that the reduction of ENO is not a simple consequence of increased ventilation nor airway obstruction. Among the EIB group, steroid-treated patients showed sooner recovery in ENO after the exercise than steroid-naive patients. Our study suggests that NO production in response to exercise may be impaired in patients with EIB, and that ENO represents not only airway inflammation but also a protective function of NO in EIB.

Administration, Inhalation↗
PubMed1996

Significance of the therapeutic range of serum theophylline concentration in the treatment of an attack of bronchial asthma.

The purpose of this study was to evaluate the accuracy of the recommended theophylline therapeutic range in the treatment of acute airway obstruction. Twenty seven patients (20 to 64 years) with acute asthma attack were given aminophylline intravenously to obtain a theophylline concentration between 10 and 20 micrograms/ml. Peak expiratory flow rates (PEFR) and serum theophylline concentrations were measured before and after aminophylline injection. When a marked improvement was not seen after aminophylline injection, the treatment was followed by inhalation of a beta-agonist and intravenously administered hydrocortisone. In order to clarify the relationship between theophylline efficacy at a therapeutic level and PEFR, as measured before aminophylline administration, the patients were classified into four groups. Group A (n = 7): asthma attack persisted regardless of treatment with aminophylline, beta-agonist and hydrocortisone, group B (n = 7): asthma attack improved by aminophylline, beta-agonist and hydrocortisone, group C (n = 6): asthma attack improved by both aminophylline and beta-agonist, group D (n = 7): asthma attack improved by intravenous aminophylline alone. The means (+/- S.E.) PEFR before aminophylline administration were 94.3 +/- 11.31/min in group A, 114.3 +/- 10.01/min in group B, 196.7 +/- 22.21/min in group C, and 220.0 +/- 12.51/min in group D, respectively. There were significant differences in PEFR between the A and C, A and D, B and C, and B and D groups. These findings suggest that theophylline efficacy is not expected in patients with low PEFR (less than 2001/min) at the time of treatment of an attack, even if a therapeutic theophylline concentration was obtained.

Adrenergic beta-Agonists↗
PubMed1988

Effects of theophylline, beta-adrenergic stimulants and prednisolone on platelet and urine cyclic guanosine monophosphate (cGMP).

Experiments were carried out to investigate the effects of anti-asthma drugs on cGMP levels. In vitro, theophylline (5 X 10(-4) M) increased basal and 5-hydroxytryptamine stimulated cGMP formation by platelets (p less than 0.05) while salbutamol and prednisolone produced no change. No significant differences were found in urine cGMP levels in healthy subjects, after short term treatment with theophylline, isoprenaline or prednisolone. Urinary cGMP levels were lower than normal in the majority (7/10) of asthma patients tested and in female patients this difference was significant (p less than 0.05). Severity of asthma symptoms were not found to be associated with particular changes in urinary cGMP levels. Fluctuations in the cGMP levels were, however, greater (p less than 0.01) in asthma patients with a more unstable respiratory condition. The differences between in vitro and in vivo results may demonstrate that beta-stimulants and theophylline have different acute and chronic effects on cGMP formation, or show that in vivo these drugs primarily affect tissue enzymes that differ from those on platelets.

Adrenergic beta-Agonists↗
PubMed2006

Effects of KP-496, a novel dual antagonist for leukotriene D4 and thromboxane A2 receptors, on contractions induced by various agonists in the guinea pig trachea.

BACKGROUND: A dry powder inhaler of KP-496 is currently in clinical development in Japan as an anti-asthmatic agent. The aim of this study was to evaluate the in vitro pharmacological profile of KP-496. METHODS: The antagonistic activities of KP-496 for leukotriene (LT) D(4) and thromboxane (TX) A(2) receptors were examined using the LTD(4)- and U46619-induced contractions of the isolated guinea pig trachea. The selectivity of KP-496 was examined using various agonist-induced contractions in the isolated guinea pig trachea. RESULTS: KP-496 produced parallel rightward shifts of the LTD(4) and U46619 concentration-response curves in a concentration-dependent manner. Schild plot analyses of the antagonistic activities of KP-496 demonstrated that it is a competitive antagonist for LTD(4) and TXA(2) receptors with pA(2) values of 8.64 and 8.23, respectively. The LTD(4) antagonistic activity of KP-496 was comparable to that of pranlukast and zafirlukast but was more potent than that of montelukast. The TXA(2) antagonistic activity of KP-496 was comparable to that of seratrodast. KP-496 and seratrodast also inhibited the prostaglandin (PG) D(2)- and PGF(2alpha)-induced contractions of the isolated guinea pig trachea. KP-496 had no effect on the histamine-, acetylcholine-, serotonin- and substance P-induced contractions of the isolated guinea pig trachea. CONCLUSIONS: These results indicate that KP-496 is a selective dual antagonist for LTD(4) and TXA(2) receptors. LTD(4) and TXA(2) play important roles in asthma, and antagonists for these mediators are being used for the treatment of asthma. Thus, KP-496 is expected to become a novel potent therapeutic agent for asthma.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1992

Premenstrual asthma with seasonal variation.

A 19-year-old woman had premenstrual asthma (PMA) usually from April through October each year with normal and regular menstrual cycles. When the monthly variation in the patient's PMA between 1984 and 1990 was compared with the monthly admissions of children for acute asthma in a hospital in this region, there was a great similarity in pattern between the two. Although she had high sensitivity to house-dust mites, the monthly pattern of her PMA did not coincide with monthly variations in the number of mites in house-dust in her home.

Administration, Inhalation↗
PubMedDate not supplied

[Beta 2 stimulants in the therapy of childhood asthma].

Bronchial obstruction, chronic or acute, is due to different anatomical and functional events, mainly to smooth muscular contraction and oedema and secretions. In the first age of life the secretions and thickness of bronchial wool are the most important factors due to small bronchial caliber and poor muscular component. In the older child the most important cause is determined by the reactive spasm of bronchial smooth muscle.

Administration, Oral↗
PubMed1984

Relationship between intrinsic activities of agonists in normal and desensitized tissue and agonist-induced loss of beta adrenergic receptors.

The intrinsic activities of 14 agonists at beta adrenergic receptors were determined in membranes prepared from control L6 muscle cells or from cells preincubated in the presence of isoproterenol for 20 min. Several drugs that were full agonists when studied with membranes from naive cells were partial agonists in membranes prepared from desensitized cells. Prolonged incubation of cells with agonists resulted in a 70 to 80% decrease in the density of beta adrenergic receptors. This effect was observed after incubation of cells with either full or partial agonists, suggesting that the extent of receptor loss is independent of the intrinsic activity of an agonist. The rate of receptor loss was related, however, to the intrinsic activity of an agonist. The rate of receptor loss correlated with the intrinsic activities of agonists in desensitized (r = 0.94) and control (r = 0.87) membranes.

Adenylyl Cyclases↗
PubMed1995

Recent trends in the use of inhaled beta 2-adrenergic agonists and inhaled corticosteroids in Saskatchewan.

OBJECTIVE: To examine recent trends in the use of inhaled beta 2-adrenergic agonists and inhaled corticosteroids for the treatment of asthma among Saskatchewan residents and to determine whether these trends are in keeping with widely publicized guidelines recommending a reduction in the use of agents to treat symptoms (i.e., inhaled beta 2-adrenergic agonists) and increased use of prophylactic agents (i.e., inhaled corticosteroids). DESIGN: Descriptive pharmacoepidemiologic study conducted with the use of data from the computerized database of the Saskatchewan Prescription Drug Plan. SETTING: Saskatchewan. PATIENTS: Saskatchewan residents 5 to 54 years of age who received one or more outpatient prescriptions for drugs to treat asthma (inhaled drugs, ingested beta 2-adrenergic agonists and ingested methylxanthines) from 1989 to 1993. OUTCOME MEASURES: Epidemiologic trends, calculated for each year: number of prescriptions per 1,000 persons; number of patients who received prescriptions for inhaled corticosteroids, inhaled beta 2-adrenergic agonists and any type of drug to treat asthma; mean number of such prescriptions per patient; and weighted mean amount of salbutamol, fenoterol and beclomethasone dispensed per patient. RESULTS: There has been an increase in the proportion of the population receiving prescriptions for drugs to treat asthma. The number of patients receiving these drugs per 1,000 people rose during the study period from 33.38 to 46.59 for any drug to treat asthma, from 24.70 to 33.77 for inhaled beta 2-adrenergic agonists and from 6.1 to 19.9 for inhaled corticosteroids. The mean number of prescriptions per patient decreased steadily for all drugs to treat asthma (from 5.34 in 1989 to 3.88 in 1993), for inhaled beta 2-adrenergic agonists (from 4.35 to 3.09) and for inhaled corticosteroids (from 2.98 to 2.25). The weighted mean amount of inhaled salbutamol dispensed per patient per year decreased by 40%, from 178.08 mg in 1989 to 109.14 mg in 1993. The weighted amount of fenoterol dispensed per patient per year declined even more, by 58%, from 387.91 mg in 1989 to 164.00 mg in 1993. Conversely, the weighted amount of inhaled beclomethasone dispensed per patient per year increased by 35% from 46.95 mg in 1989 to 63.50 mg in 1992, then dropped to 56.17 mg per year in 1993. CONCLUSION: These data demonstrate a substantial change in Saskatchewan in the prescribing of drugs to treat asthma; they suggest that many physicians responded to current guidelines advocating increased attention to prevention of airway inflammation in the treatment of asthma.

Administration, Inhalation↗
PubMedDate not supplied

Increased plasma level of platelet-activating factor (PAF) and decreased serum PAF acetylhydrolase (PAFAH) activity in adults with bronchial asthma.

We evaluated the plasma level of platelet-activating factor (PAF), a chemical mediator that induces various symptoms of bronchial asthma, and the activity of serum PAF acetylhydrolase (PAFAH), an enzyme that specifically inactivates PAF, in adults with bronchial asthma. Measurements were made by radioimmunoassay of samples obtained from 137 adult asthmatic patients (137 cases examined in remission and from among these 41 cases were also measured at the time of an asthmatic attack) 59 adult patients with untreated pulmonary tuberculosis and 106 healthy adult volunteers. It was demonstrated that the plasma PAF level was markedly higher and the serum PAFAH activity markedly lower in the asthmatic patients, both in remission and at the time of asthmatic attack, than in the healthy volunteers. The plasma PAF level was more closely associated with asthma both in remission and at the time of asthmatic attack than with pulmonary tuberculosis, whereas there was no significant difference in the serum PAFAH activity between the two diseases. The low serum PAFAH activity in the asthmatic patients may have been due to saturation as a result of continuous reaction to the increased plasma PAF level in those patients.

1-Alkyl-2-acetylglycerophosphocholine Esterase↗