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PubMed1993

Protective effect of SV-IV on platelet-activating factor-induced hypotension, bronchoconstriction and gastric mucosal injury.

The inhibitory effect of one of the major proteins secreted by the rat seminal vesicles (SV-IV) on platelet-activating factor (PAF)-induced biological activities was investigated in vivo. SV-IV was found to prevent dose dependently both hypotension and acute bronchospasm caused by PAF administration in guinea-pigs. In addition, SV-IV inhibited both PAF- and ethanol-induced gastric mucosal injury in a dose-dependent manner.

Animals↗
PubMed1995

Effect of bronchoconstrictive aerosols on pulmonary gas trapping in the A/J mouse.

We exposed A/J mice to several challenge aerosols and measured gas trapped within excised lungs by quantitating their buoyancy in saline (Archimedes' principle). The temporal stability of the excised lung gas volume (ELGV) measurement was also examined. ELGV increased in a dose proportional manner with increasing concentrations of methacholine and reached a maximum of 338 +/- 33% above vehicle-exposed controls. The A/J mice were 100 times more responsive to aerosol methacholine compared to hyporesponsive C3H/HeJ mice. Aerosol challenges of U-46619, a thromboxane A2 mimetic, and serotonin resulted in a 40% and 135% increase in ELGV's versus their controls, respectively. ELGV's were not increased after aerosols of leukotriene C4, histamine, substance P, N-formyl-methionyl-leucyl-phenyl-alanine and platelet activating factor. Both normal (filtered air-exposed) and hyperinflated (methacholine-exposed) excised lungs lost about 10% of their initial volume by 30 min and 40-65% of initial volume by 4 h. Occlusion of the trachea in either group did not affect the total gas lost, suggesting that majority of the gas loss was via transpleural diffusion. We conclude that determination of ELGV in mice, when performed soon after challenge testing, is a simple, rapid and reliable estimate of airway obstruction.

Aerosols↗
PubMed1991

Near-fatal asthma: clinical and physiologic features, perception of bronchoconstriction, and psychologic profile.

We studied 19 subjects with asthma (11 men and eight women, aged 20 to 66 years), 6 months to 5 years after a near-fatal (NF) episode of asthma (NF group). Mean duration of asthma was 16.3 +/- 2.4 years. On reevaluation, all subjects were using an inhaled beta 2-agonist and inhaled steroids (mean daily dose of budesonide, 1070 micrograms [N = 5], and beclomethasone, 1079 micrograms [N = 14]). Two subjects were taking prednisone, 10 and 15 mg/day. Subjects were matched for age, sex, atopic status, baseline FEV1, and medication use to a control group (C group) of subjects with asthma who had never experienced an NF asthma episode. All subjects had the following evaluation: (1) questionnaire on the characteristics of their asthma, (2) spirometry, (3) morning and evening measurements of peak expiratory flow rates (PEFR) with daily recordings of asthma symptoms for 4 weeks, and (4) psychometric evaluation with the Minnesota Multiphasic Personality Inventory. Ten subjects of the NF group and 13 of the C group had a methacholine challenge with scoring of dyspnea on a modified Borg scale. Mean percent predicted (+/- SEM), FEV1, FVC, and PEFR were similar for the NF and C groups with respective values of 63.4 (4.4), 61.3 (5.6), 81.1 (4.5), 79.1 (3.8), 61.3 (5.6), and 62.4 (6.1). Geometric mean of the provocative concentration of methacholine causing a 20% drop in FEV1 (milligrams per milliliter) was 0.61 for the NF group (N = 10) and 1.18 for the C group (N = 13).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1992

Salmeterol, a new inhaled beta 2-adrenergic agonist, has a longer blocking effect than albuterol on hyperventilation-induced bronchoconstriction.

The duration of the blocking effect of salmeterol (50 micrograms), albuterol (200 micrograms), and a placebo were compared in a double-blind study in 12 adult subjects with asthma who underwent hyperventilation tests with cold dry air (-20 degrees C) on 4 study days. On the first day, the hyperventilation test was performed at various time intervals (baseline, 1, 4, 6, 8, 12, and 24 hours) with spontaneous functional recovery between each test to determine the within-day within-subject variability of the response. The response was assessed by interpolating the dose of cold dry air causing a 20% fall in FEV1. On the 3 remaining days, separated by an interval of at least 5 days, the active or placebo medication was administered after spontaneous recovery from the first hyperventilation test. Spirometry was assessed 15 minutes and 1 hour later. The hyperventilation test was then performed and repeated 4 hours after administration of the drug. The test was repeated 6, 8, 12, and 24 hours later to detect any significant blocking effect. The improvement in FEV1 15 minutes and 1 hour after the drug was administered was 19.8% and 20.4%, as compared to baseline for albuterol, and 16.3% and 16.8% for salmeterol (not significant). The mean duration of the blocking effect was 0.25 hour for the placebo, 3.5 hours for albuterol, and 15.9 hours for salmeterol (F = 24.5; p less than 0.001; Newman-Keul's test was significant for every contrast). Eight of the 12 subjects still demonstrated some blocking effect 8 hours after taking salmeterol; this was true for only one subject receiving albuterol.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

The effect of an oral leukotriene antagonist, ONO-1078, on allergen-induced immediate bronchoconstriction in asthmatic subjects.

BACKGROUND: Cysteinyl leukotrienes are potent contractile agonists for airway smooth muscle. To examine the relative role of cysteinyl leukotrienes in immediate airway obstruction in human subjects with asthma after allergen challenge, we investigated the effect of ONO-1078, a potent receptor antagonist of cysteinyl leukotrienes, on the response. METHODS: ONO-1078 and an inactive placebo, in 150-mg capsule form, were administered every 12 hours for 1 week, in a double-blind, cross-over fashion. To examine the effect on the early part of the response, total respiratory resistance (Rrs) was continuously evaluated for 10 minutes after the start of a 1-minute exposure to an appropriate concentration of allergen. Rrs and FEV1.0 were estimated every 10 minutes for 60 minutes after the exposure. RESULTS: ONO-1078 significantly reduced percent changes in Rrs and FEV1.0 from 20 to 60 minutes after the exposure, as well as percent maximum changes in these indices, although the treatment did not alter the time from the start of allergen exposure to the beginning of elevation of Rrs, the time from the start to the point at which total respiratory conductance decreased by 35% from its baseline value, or percent changes in Rrs or FEV1.0 10 minutes after the exposure. CONCLUSIONS: Therefore, we conclude that cysteinyl leukotrienes primarily mediate a later part of immediate airway obstruction after allergen exposure.

Administration, Oral↗
PubMed1993

The effect of H1-receptor blockade on the development of early- and late-phase bronchoconstriction and increased bronchial responsiveness in allergen-induced asthma.

BACKGROUND: Allergen challenge of subjects with asthma produces an early asthmatic response, late asthmatic response, and increases bronchial responsiveness. Histamine partly mediates the early asthmatic response, and may play a role in late-phase responses. Azelastine has antiallergic properties and has been proposed as a treatment for asthma. We therefore investigated the contribution of histamine to late-phase responses with the use of the potent H1-receptor antagonist azelastine. METHODS: Ten subjects with atopic asthma were studied in a double-blind, randomized, placebo-controlled trial. Azelastine was administered over 4 days before allergen challenge. Changes in airway caliber were followed with measurements of forced expiratory volume in 1 second, and changes in bronchial responsiveness were followed by methacholine and prostaglandin D2 bronchial provocation tests. RESULTS: Azelastine significantly inhibited the development of the early asthmatic response. Azelastine had no effect on the late asthmatic response or on the development of allergen-induced increases in bronchial responsiveness. The power of the study was sufficient to have had a high probability of detecting any important differences between placebo and azelastine during the late phase. CONCLUSIONS: Azelastine had no significant effect on the late-phase response model of asthma. This study does not support the hypothesis that histamine is an important mediator of the late asthmatic response or allergen-induced increases in bronchial responsiveness.

Adult↗
PubMed1990

Neuropeptide Y modulates non-adrenergic, non-cholinergic neural bronchoconstriction in vivo and in vitro.

Non-adrenergic, non-cholinergic (NANC) neural mechanisms regulate airway tone in guinea-pigs, and it is possible that they may be regulated by other nerves. We have investigated effects of neuropeptide Y (NPY), a co-transmitter of adrenergic nerves, on the excitatory (bronchoconstrictor) NANC (e-NANC) response elicited both in vivo (via bilateral vagal nerve stimulation) and in vitro (via electrical field stimulation [EFS]), and on inhibitory (bronchodilator) NANC (i-NANC) responses in upper trachea elicited by EFS. NPY inhibited the e-NANC to vagal stimulation in vivo in a dose-dependent manner (90.0 +/- 3.4% inhibition at 500 micrograms/kg), but failed to alter the bronchoconstrictor response to exogenous substance P (SP). NPY also inhibited the e-NANC response to EFS in main and hilar bronchi (57.2 +/- 8.6% in main and 46.34 +/- 7.5% in hilar bronchi at 10(-6) M), whilst having no effect on the contractile response to SP. In contrast NPY had no effect on the i-NANC response in vitro. Thus, NPY exerts a powerful inhibitory action on tachykinin release from peripheral endings of capsaicin-sensitive airway sensory nerves, but has no effect on the i-NANC neural mechanisms. This suggests that adrenergic nerves may modulate e-NANC responses in the airways.

Animals↗
PubMed1995

Aspirin, salicylate, sulfite and tartrazine induced bronchoconstriction. Safe doses and case definition in epidemiological studies.

Allergic-like reactions to chemical components of foods and medicines may be common. The prevalence of idiosyncratic reactions to aspirin, salicylate, metabisulfite and tartrazine is not known. We used a tertiary referral clinic population to estimate safe exposure doses for epidemiological studies. A 15% decrease in the amount of air expired in one second was defined a positive response. The median effective molar doses of the agents were remarkably similar: metabisulfite 0.19 mM, 34.4 mg [95% confidence interval (CI) 0.14, 0.27 mM]; tartrazine 0.10 M, 55.0 mg (95% CI 0.05, 0.21 mM); aspirin 0.09 mM, 16.5 mg (95% CI 0.04, 0.19 mM); and salicylate 0.11 mM, 15.3 mg (95% CI 0.05, 0.27 mM). Doses to which the most sensitive (5%) and practically all (95%) susceptible persons might respectively respond are: metabisulfite 4.6 mg, 255.8 mg; tartrazine 3.4 mg, 885.6 mg; aspirin 0.8 mg, 332.3 mg; and salicylate 2.6 mg, 89.9 mg. Doses within these ranges can be used in epidemiological studies.

Adolescent↗
PubMed1991

Inhibition by Ro 31-6930 of agonist and allergen induced bronchoconstriction in anaesthetised guinea-pigs and cats.

Ro 31-6930, a potent smooth muscle relaxant from the novel class of potassium channel openers, has been compared with BRL 38227, salmeterol and theophylline in a range of models of airway function. Ro 31-6930 relaxed isolated tracheal muscle from sensitised guinea-pigs which had been contracted by ovalbumin and was equipotent with salmeterol in inhibiting antigen-induced bronchospasm in anaesthetised, sensitised guinea-pigs. In both anaesthetised guinea-pig and cat, Ro 31-6930, BRL 38227 and theophylline were more potent against 5-HT evoked increases in lung resistance than they were on falls in dynamic compliance. Although salmeterol had equivalent activity on both parameters it is unlikely that the small difference seen with the other compounds reflect a preferential effect on large airways. In addition, Ro 31-6930 was an effective bronchodilator when given by inhalation to the anaesthetised guinea-pig. In view of the protective activity of Ro 31-6930 against antigen challenge in the sensitised guinea-pig and its potency in relation to other bronchodilators, it is considered that compounds which relax airway smooth muscle by the opening of plasmalemmal potassium channels may have a role in the treatment of asthma.

Aerosols↗
PubMed1991

Influence of aminophylline and ketotifen in comparison to the lipoxygenase inhibitors NDGA and esculetin and the PAF antagonists WEB 2170 [correction of 2107] and BN 52021 on endothelin-1 induced vaso- and bronchoconstriction.

Theophylline (p less than 0.05) and ketotifen (p greater than 0.05) markedly reduced, but the lipoxygenase inhibitors and PAF receptor antagonists were without any influence on the endothelin-1 (ET-1 1 nmol/kg i.v.) induced increase of pulmonary inflation pressure of anaesthetised and ventilated guinea-pigs. The ET-1 induced increase in mean arterial blood pressure as well as the secondary TXB2 release into bronchoalveolar lavage fluid or plasma was not decreased. TXB2 release cannot be the only mechanism of bronchopulmonary ET-1 effects in guinea-pigs in vivo.

Aminophylline↗
PubMed1995

Inhaled nitric oxide reverses PAF-dependent bronchoconstriction in the pig.

In six anesthetized, paralyzed, mechanically ventilated pigs we evaluated the respiratory effects of inhaled nitric oxide (NO) (80 ppm in O2) under control conditions and after platelet-activating factor (PAF) administration (50 ng/kg, i.v.). PAF was also administered to the same pigs after pretreatment with indomethacin (3 mg/kg, i.v.). The mechanical properties of the respiratory system were evaluated by the rapid airway occlusion technique. With this technique the overall respiratory resistances, the airway resistances, and the additional resistances of respiratory system and lung can be evaluated. The results show that NO inhaled by the pig at 80 ppm for 6 min under control conditions reduced static and dynamic elastances of the respiratory system and lung and pulmonary arterial pressure, without modifying bronchomotor tone. Therefore, NO reduced the PAF-dependent changes in resistances and in static and dynamic elastances of the respiratory system and lung. The modest change in elastances caused by PAF in pigs pretreated with indomethacin was reduced by NO inhalation, which also has a mild bronchodilatory effect. The changes in elastances appear to be correlated with the pulmonary vasodilator activity of inhaled NO.

Administration, Inhalation↗