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PubMed1992

Bronchoconstriction and airway microvascular leakage in guinea pigs sensitized with trimellitic anhydride.

We have developed a guinea pig model of immediate airway responses following intradermal sensitization with free trimellitic anhydride (TMA). Guinea pigs were given an intradermal injection with either 0.1 ml of 0.3% TMA in corn oil (n = 8) or 0.1 ml of corn oil alone (n = 6). A guinea pig serum albumin conjugate of trimellitic anhydride (TMA-GPSA) was prepared with a substitution ratio of 21:1. All sensitized guinea pigs had raised specific serum IgG1 antibodies (ELISA), and IgE antibodies were detected in six of the eight sensitized guinea pigs by passive cutaneous anaphylaxis. On Days 21 to 28, guinea pigs were anesthetized, tracheostomized, and ventilated. Evans blue dye (20 mg/ml), an albumin marker, was injected intravenously to quantify airway microvascular leakage (MVL). TMA-GPSA (50 microliters; 1%) in saline was instilled into the trachea. Lung resistance (RL) was measured for 6 min. The guinea pigs were killed, and the lungs were removed. Peak RL (cm H2O/ml x s-1) was significantly increased in sensitized guinea pigs from 0.26 +/- 0.01, mean +/- SEM to 21.3 +/- 6.9 (p < 0.05), compared with nonsensitized guinea pigs. There was a significant increase in Evans blue at all levels of the tracheobronchial tree in sensitized guinea pigs compared with the controls (p < 0.005). The site of MVL was localized to the postcapillary venules as assessed by extravasation of intravascular Monastral blue dye. We conclude that intradermal sensitization of guinea pigs to TMA induces a polyclonal immune response, associated with bronchoconstriction and airway microvascular leakage, when challenged specifically with TMA-GPSA.(ABSTRACT TRUNCATED AT 250 WORDS)

Airway Resistance↗
PubMed1993

Potent leukotriene D4 receptor antagonist ICI 204,219 given by the inhaled route inhibits the early but not the late phase of allergen-induced bronchoconstriction.

ICI 204,219 is a potent and specific leukotriene D4 receptor antagonist that blocks both the early and late responses to allergen challenge in humans when given orally at a dose of 40 mg. Here we report our findings with an inhaled formulation of ICI 204,219 against allergen-induced bronchoconstriction. A group of 10 atopic subjects (mean age 25.6 +/- 4.2; 6 females; FEV1 > 90% of predicted; on inhaled beta 2-agonists only) were studied on 2 separate days 2 to 3 wk apart. In a randomized placebo-controlled trial they inhaled eight puffs of a standard metered dose inhaler containing either ICI 204,219 (200 micrograms/puff, total dose 1,600 micrograms) or propellant alone. They underwent bronchial allergen challenge 30 min later using a single concentration of allergen previously shown to lower the FEV1 by > or = 15%. FEV1 was monitored hourly for 10 h, and urine was collected for LTE4 determination. Inhalation of ICI 204,219 was well tolerated, with no adverse clinical or biochemical effects. There was no significant effect of ICI 204,219 inhalation on basal airway caliber (change in FEV1 30 min after inhalation was -149 +/- 67 ml after placebo versus 3 +/- 38 ml after ICI 204,219; p = 0.08). The early response to allergen was significantly inhibited by ICI 204,219 (the maximum fall in FEV1 was -21.2 +/- 6.1% after ICI 204,219 compared with -38.8 +/- 6.5% on placebo; p = 0.007).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed2003

Neurokinins modulate hyperventilation-induced bronchoconstriction in canine peripheral airways.

This study was designed to test the hypotheses that (1) neurokinin (NK) receptor activity modulates hyperventilation-induced bronchoconstriction (HIB) in canine peripheral airways and (2) NK receptor activity is stimulated via hyperventilation-induced eicosanoid production and release. A bronchoscope was used in anesthetized dogs to record peripheral airway resistance (Rp); to test airway reactivity to NK A (NKA), substance P, and hypertonic saline; and to examine HIB before and after combined treatment with NK-1 (CP 99,994) and NK-2 (SR 48,968) receptor antagonists. Bronchoalveolar lavage fluid cells, prostaglandin D2, and cysteinyl leukotrienes from hyperventilated airways pretreated with either vehicle or NK antagonists were also measured. Pretreatment with NK-1 and NK-2 antagonists significantly attenuated HIB and the response to substance P, virtually abolished the response to NKA, and had little effect on the response to HS. Blockade of NK-1 and NK-2 receptors did not affect either the cell profiles or the mediator concentrations recovered in bronchoalveolar lavage fluid after hyperventilation. We conclude that NKs modulate the development of HIB and appear to do so via hyperventilation-induced eicosanoid production and release.

Animals↗
PubMed2005

Inflammatory basis of exercise-induced bronchoconstriction.

RATIONALE: Exercise-induced bronchoconstriction (EIB) is a highly prevalent condition with unclear pathogenesis. Two competing theories of the pathogenesis of EIB differ regarding the inflammatory basis of this condition. OBJECTIVES: Our goals were to establish whether epithelial cell and mast cell activation with release of inflammatory mediators occurs during EIB and how histamine and cysteinyl leukotriene antagonists alter the airway events occurring during EIB. METHODS: Induced sputum was used to measure mast cell mediators and eicosanoids at baseline and 30 minutes after exercise challenge in 25 individuals with asthma with EIB. In a randomized, double-blind crossover study, the cysteinyl leukotriene antagonist montelukast and antihistamine loratadine or two matched placebos were administered for two doses before exercise challenge. MAIN RESULTS: The percentage of columnar epithelial cells in induced sputum at baseline was associated with the severity of EIB. After exercise challenge, histamine, tryptase, and cysteinyl leukotrienes significantly increased and prostaglandin E(2) and thromboxane B(2) significantly decreased in the airways, and there was an increase in columnar epithelial cells in the airways. The concentration of columnar epithelial cells was associated with the levels of histamine and cysteinyl leukotrienes in the airways. Treatment with montelukast and loratadine inhibited the release of cysteinyl leukotrienes and histamine into the airways, but did not inhibit the release of columnar epithelial cells into the airways. CONCLUSIONS: These data indicate that epithelial cells, mast cell mediators, and eicosanoids are released into the airways during EIB, supporting an inflammatory basis for EIB.

Acetates↗
PubMed1991

Lipopolysaccharide from Escherichia coli reduces antigen-induced bronchoconstriction in actively sensitized guinea pigs.

Bronchoconstriction (BC) is the main feature of anaphylaxis in the guinea pig. Since LPS induces lung inflammation and antigen-induced BC depends on the endogenous formation of histamine and arachidonate metabolites, we studied whether LPS might modulate antigen-induced BC. Guinea pigs were sensitized subcutaneously with 10 micrograms ovalbumin (OA) on days 0 and 14. LPS (100 micrograms/kg) was injected intravenously on day 21, and daily injections of LPS were continued before the antigenic challenge on day 22, 23, 24, or 25. Intratracheal injection of 100 micrograms OA induced an abrupt and reversible BC. Single or repetitive injections of LPS reduced BC. LPS is likely to reduce the OA-induced BC by affecting the histamine-dependent component of BC, since (a) LPS induced a partial degranulation of lung mast cells; (b) BC is reduced by mepyramine, an histamine receptor antagonist; (c) LPS did not affect BC in mepyramine-treated guinea pigs; (d) LPS reduced histamine release by OA-stimulated guinea pig lungs in vitro. Moreover, the in vitro OA-induced production of arachidonate metabolites was also reduced by LPS. The decreased formation of TXB2 was not only secondary to a reduced release of histamine, since LPS inhibited TXB2 formation in the presence of mepyramine. Finally, the FMLP-induced BC and mediator release were inhibited by LPS, whereas the platelet activating factor-induced pulmonary responses were not. Thus, the protective effect of LPS is not antigen-specific and does not result from a general desensitization. These studies indicate that a single dose of LPS reduces the antigen-induced BC by reducing histamine release from lung mast cells, although a decreased formation of eicosanoids may contribute to the protective effect of LPS.

Animals↗
PubMedDate not supplied

Baclofen-induced bronchoconstriction.

OBJECTIVE: To report the occurrence of acute bronchospasm in one asthmatic patient and increased bronchial reactivity in another following the administration of a single dose of oral baclofen. CASE SUMMARY: On two separate occasions, a 46-year-old asymptomatic asthmatic man developed dyspnea and chest tightness one hour after the ingestion of baclofen 40 mg. Pulmonary function studies revealed a significant decrease in airflow relative to baseline. A 33-year-old asymptomatic woman with a history of exercise-induced dyspnea and wheezing displayed bronchial hyperresponsiveness to inhaled metacholine 2 hours after ingesting 40 mg of baclofen. The patient had had a negative methacholine challenge test 72 hours earlier. DISCUSSION: The gamma-aminobutyric acid-agonist baclofen has been shown to reduce airway responsiveness to various bronchoconstricting agents in animal studies. The etiology of this seemingly paradoxical response in two patients is unclear, but may offer insight into the neurally mediated airway constriction that occurs in asthma. CONCLUSIONS: Clinicians should be aware of the possibility of baclofen-induced bronchospasm, especially in asthmatic patients.

Adult↗
PubMed2001

Bronchoconstriction induced by inhaled adenosine 5'-monophosphate in subjects with allergic rhinitis.

Adenosine and its related nucleotide, adenosine 5'-monophosphate (AMP) induce bronchoconstriction in asthmatics, probably caused by histamine release from airway mast cells. The objective of this study was to determine the effect of inhaled AMP on lung function in subjects with allergic rhinitis. A total of 52 adults (28 subjects with allergic rhinitis, 14 asthmatics and 10 healthy subjects) were challenged with increasing concentrations of AMP and methacholine. Airflow was assessed after each concentration and the response to each bronchoconstrictor agent was measured by the provocative concentration required to produce a 20% fall (PC20) in forced expired volume in one second (FEV1). All 14 asthmatics, 10 subjects with allergic rhinitis and none of the healthy controls were hyperresponsive to AMP. Subjects with allergic rhinitis had higher prevalence of hyperresponsiveness to AMP than healthy controls (p=0.038). Although the prevalence of hyperresponsiveness for methacholine and for AMP in subjects with allergic rhinitis was similar (39% and 36%, respectively), four subjects had hyperresponsiveness to methacholine but not to AMP, whereas three subjects had hyperresponsiveness to AMP but not to methacholine. To conclude, inhaled adenosine 5'-monophosphate causes airway narrowing in a significantly higher proportion of subjects with allergic rhinitis than healthy volunteers. Furthermore, methacholine and adenosine 5'-monophosphate hyperresponsiveness are not detected in the same individuals with allergic rhinitis, thus suggesting that responsiveness to the two bronchoconstrictor stimuli is not reflecting the same abnormalities of the airways.

Adenosine Monophosphate↗
PubMed2001

Reversing acute bronchoconstriction in asthma: the effect of bronchodilator tolerance after treatment with formoterol.

Continuous treatment with a short-acting beta2-agonist can lead to reduced bronchodilator responsiveness during acute bronchoconstriction. This study evaluated bronchodilator tolerance to salbutamol following regular treatment with a long-acting beta2-agonist, formoterol. The modifying effect of intravenous corticosteroid was also studied. Ten asthmatic subjects (using inhaled steroids) participated in a randomised, double-blind, placebo-controlled, cross-over study. Formoterol 12 microg b.i.d. or matching placebo was given for 10-14 days with >2 weeks washout. Following each treatment, patients underwent a methacholine challenge to induce a fall in forced expired volume in one second (FEV1) of at least 20%, then salbutamol 100 microg, 100 microg, and 200 microg was inhaled via a spacer at 5 min intervals, with a further 400 microg at 45 min. After a third single-blind formoterol treatment period, hydrocortisone 200 mg was given intravenously prior to salbutamol. Dose-response curves for change in FEV1 with salbutamol were compared using analysis of covariance to take account of methacholine-induced changes in spirometry. Regular formoterol resulted in a significantly lower FEV1 after salbutamol at each time point compared to placebo (p<0.01). The area under the curves (AUCs) for 15 (AUC0-15) and 45 (AUC0-45) min were 28.8% and 29.5% lower following formoterol treatment (p<0.001). Pretreatment with hydrocortisone had no significant modifying effect within 2 h of administration. It is concluded that significant tolerance to the bronchodilator effects of inhaled salbutamol occurs 36 h after stopping the regular administration of formoterol. This bronchodilator tolerance is evident in circumstances of acute bronchconstriction.

Acute Disease↗
PubMed2001

The reproducibility and sample size requirements of exercise-induced bronchoconstriction measurements.

Dry air exercise challenges are frequently used to screen medications that have potential utility in the management of exercise-induced bronchoconstriction (EIB). The purpose of this study was to determine the reproducibility of three outcome measurements made using such challenges, and sample size requirements for drug evaluation studies based on these outcomes. Forty adult subjects with asthma, who tested positively on a screening exercise challenge, were subjected to two further identical challenges, separated by 1 to >35 days. Outcome measurements included the maximum per cent fall in forced expiratory volume in one second (FEV1), after exercise (% fallmax), and the area under the per cent fall in FEV1/time curve for 30 min (AUC30) and 60 min (AUC60) after exercise. The reproducibility of these outcomes, as assessed by intraclass correlation coefficients was 0.72, 0.53 and 0.35 for % fallmax, AUC30 and AUC60 measurements, respectively. The sample size requirements to demonstrate an attenuation of EIB equivalent to a 50% reduction in % fallmax was 9, 14 and 19 subjects for the % fallmax, AUC30 and AUC60 responses, respectively (90% power). It is concluded that the maximum percentage fall in forced expiratory volume in one second has greater reproducibility and results in greater power in clinical trials than area under the curve measurements. Sample size calculation curves are provided which may be used in study design and interpretation of published studies.

Adult↗
PubMed2004

Exaggerated bronchoconstriction due to inhalation challenges with occupational agents.

Inhalation challenges with occupational agents are used to confirm the aetiology of occupational asthma. It has been proposed that using closed-circuit equipment rather than the realistic challenge method would improve the methodology of these tests. Changes in forced expiratory volume in one second (FEV1) were examined in 496 subjects with "positive specific inhalation challenges", i.e. changes in FEVI of > or = 20% after exposure to an occupational agent, including 357 subjects exposed by the realistic method, 108 using the closed-circuit method and 31 by both methods. For immediate reactions, 18 of 95 (19%) showed changes in FEV1 of > or = 30% with the closed-circuit method, whereas a significantly larger proportion, i.e. 77 of 200 (38.5%), showed such changes using the realistic method. As regards nonimmediate reactions, changes in FEV1 of > or = 30% occurred in 16 of 43 (37%) cases with the closed-circuit method as compared to a larger proportion, i.e. 87 of 180 (48%) cases, using the realistic method. This favourable effect was significantly more pronounced in workers with higher levels of bronchial hyperresponsiveness to methacholine. It is concluded that, for agents that can be generated using the closed-circuit method, use of such apparatus results in a smaller proportion of exaggerated bronchoconstriction than does the realistic method, this being particularly true for low-molecular weight agents.

Administration, Inhalation↗
PubMed1994

Hypothesis: excessive bronchoconstriction in asthma is due to decreased airway elastance.

Based on the strikingly different mechanical properties of airway smooth muscle preparations of different species, we hypothesized that a decrease in the elastance of nonmuscle elements within airway walls of asthmatics reduces the load limiting smooth muscle shortening, thereby allowing excessive smooth muscle shortening and bronchoconstriction. Full thickness, circumferentially cut, lobar bronchial preparations were obtained from one asthmatic and six nonasthmatic lobectomy subjects. Passive tension of the asthmatic preparation was less than that for any nonasthmatic preparation at all lengths below that for optimal force generation (Lmax). Maximal isometric force generation was greater in the asthmatic specimen (2.32 g) than in the nonasthmatic specimens (0.90 +/- 0.15 g), with stress threefold higher for the asthmatic tissue. Isotonic shortening of the asthmatic preparation was strikingly greater at starting lengths less than or equal to Lmax, with maximal fractional shortening being 31% versus 11 +/- 2% for nonasthmatic preparations. Morphometric analysis revealed no differences in cross-sectional areas of smooth muscle for asthmatic versus nonasthmatic preparations. We conclude that the reduced tissue elastance may account for the greater muscle shortening by placing a lesser load upon the smooth muscle. Airway inflammation in asthma may alter connective tissue matrix elements within airway walls leading to this decreased elastance and excessive smooth muscle shortening.

Aged↗
PubMed1995

Prostaglandin D2-induced bronchoconstriction is mediated only in part by the thromboxane prostanoid receptor.

Prostaglandin D2 (PGD2) is a potent bronchoconstrictor, and is thought to have a role in the pathogenesis of asthma. PGD2 causes vasodilation acting via the prostaglandin (DP) receptor on vascular smooth muscle, and myocontraction acting via the thromboxane (TP) receptor on bronchial smooth muscle. To determine the relative contribution of these mechanisms we have studied the degree to which a potent TP receptor antagonist inhibits PGD2-induced bronchoconstriction. Twelve atopic asthmatic subjects underwent baseline PGD2 bronchial challenges to determine the cumulative concentration of PGD2 required to reduce forced expiratory volume in one second (FEV1) by 20%. At four subsequent randomized visits, subjects received this concentration of PGD2 90 min after dosing with placebo or 20, 50 or 100 mg of BAY u 3405, a potent competitive TP receptor antagonist. Serum was taken for drug assay at 90 min. After each dose of PGD2, FEV1 was measured for 30 min, and the area under the percentage fall in the FEV1/time curve (AUC) was calculated. The mean +/- SEM AUC for placebo was 414 +/- 68, and for the 20, 50 and 100 mg doses of BAY u 3405 was 169 +/- 33, 173 +/- 59 and 135 +/- 63, respectively. There were no significant differences between the AUCs for any of the drug doses, whilst all three doses were significantly different from placebo. The plateau response achieved with increasing doses of the antagonist suggests complete blockade of the TP receptor. These data demonstrate that thromboxane receptor blockade only partially inhibits the airway narrowing response to PGD2, and support the existence of a vascular component to PGD2-induced acute airway narrowing in asthma.

Adult↗
PubMed1998

Increases in airway eosinophils and interleukin-5 with minimal bronchoconstriction during repeated low-dose allergen challenge in atopic asthmatics.

Repeated low-dose allergen challenge increases airway hyperresponsiveness in atopic asthmatics. However, it is not known whether low-dose allergen challenge increases airway inflammation. Eight atopic asthmatics were enrolled in a controlled, cross-over study to evaluate the effect and time course of repeated low-dose allergen challenge on airway inflammation and hyperresponsiveness. The dose of allergen to reduce forced expiratory volume in one second (FEV1) by approximately 5% was selected in a screening allergen challenge. The subjects then were challenged for five consecutive days with either diluent or the selected low-dose of allergen. Methacholine airway hyperresponsiveness (PC20,meth) was measured and sputum induced on days 1, 3 and 5 of the repeated challenge, and then 1 day and 3 days after the last challenge. Repeated low-dose allergen challenge caused small reductions in FEV1, but increased airway eosinophils and interleukin (IL)-5, airway hyperresponsiveness, asthma symptoms and beta2-agonist use, all of which peaked on days 3 or 5 of the challenge. The mean (SEM) percentage sputum eosinophils was 21.2 (0.7)% after allergen versus 3.9 (0.1)% after diluent (p<0.001); percentage EG2+ cells were 13.4 (03)% after allergen versus 1.1 (0.04)% after diluent (p<0.01) and geometric mean (GSEM) eosinophil cationic protein (ECP) was 1061.8 (1.6) microg x L(-1) after allergen versus 447.03 (1.2) microg x L(-1) after diluent (p<0.05). Geometric mean (GSEM) IL-5 was 71.4 (1.4) pg x mL(-1) after allergen versus 18.4 (1.04) pg x mL(-1) after diluent (p<0.01). All the changes had resolved by 3 days after the last challenges. The study demonstrated that repeated inhalation of a low-dose of allergen causes airway eosinophilia and increases in interleukin-5, associated with airway hyperresponsiveness, and mild worsening of asthma control, without the development of marked acute bronchoconstriction or the development of late responses.

Adult↗
PubMed2006

Onset of relief of dyspnoea with budesonide/formoterol or salbutamol following methacholine-induced severe bronchoconstriction in adults with asthma: a double-blind, placebo-controlled study.

BACKGROUND: The long-acting beta2-agonist (LABA) formoterol has an onset of effect comparable to that of salbutamol. Consequently, the combination of formoterol and budesonide in one inhaler, approved for maintenance use, can potentially be used for reliever therapy. This study compared the onset of relief from induced bronchospasm with a single dose of budesonide/formoterol versus standard salbutamol therapy in patients with asthma. METHODS: In this randomised, double-blind, placebo-controlled, cross-over study, 32 patients with asthma underwent a methacholine provocation test leading to a fall in forced expiratory volume in 1 second (FEV1) of > or =30% at enrollment (Visit 1) and three subsequent study visits (Visits 2-4). Immediately after each provocation at Visits 2-4, patients received one of three test treatments: one inhalation of budesonide/formoterol 160/4.5 microg (via Turbuhaler), two inhalations of salbutamol 100 microg (via a pressurised metered-dose inhaler [pMDI]) or placebo. All patients received each of the test treatments in a randomised order, after separate methacholine provocations. The effect of treatment on FEV1 and breathlessness (using the Borg scale) was measured at 1, 3, 5, 10, 15, 20, 25 and 30 minutes after test treatment. RESULTS: Following methacholine provocation, Borg score increased from a baseline value of below 0.5 to 3.03, 3.31 and 3.50 before treatment with budesonide/formoterol, salbutamol and placebo, respectively. Budesonide/formoterol and salbutamol reversed methacholine-induced dyspnoea (breathlessness) rapidly. At 1 minute after inhalation, statistically significant decreases in Borg score were observed for budesonide/formoterol and salbutamol (p = 0.0233 and p < 0.0001, respectively, versus placebo), with similar rapid increases in FEV1 (both active treatments p < 0.0001 versus placebo). The median time to 50% recovery in Borg score after methacholine provocation was 3 minutes with budesonide/formoterol, 2 minutes with salbutamol and 10 minutes with placebo. All treatments and procedures were well tolerated. CONCLUSION: Single doses of budesonide/formoterol and salbutamol both provided rapid relief of dyspnoea and reversal of severe airway obstruction in patients with asthma with experimentally induced bronchoconstriction. The perception of relief, as confirmed by objective lung function assessment, provides evidence that budesonide/formoterol can be used as reliever medication in asthma.

Adolescent↗
PubMed2004

Facial cooling enhances exercise-induced bronchoconstriction in asthmatic children.

PURPOSE: Exercising in cold air enhances bronchial responsiveness (BR) as compared with exercising in warm air. This may be due to intrathoracic cooling or to increased vagal activity caused by facial cooling. The purpose of this study was to compare the effects on BR of cold air inhalation and of facial exposure to cold air, as well as the combined effect of both. METHODS: Fourteen children with asthma (eight girls) performed four exercise challenge tests in a climatic chamber, under one of the following conditions: 1) inhaling warm air while the face was exposed to warm air (WW, 21 degrees C, 25% relative humidity (RH)); 2) inhaling warm air while the face was exposed to cold air (WC, 0 degrees C, 80% RH); 3) inhaling cold air while the face was exposed to cold air (CC); and 4) inhaling cold air while the face was exposed to warm air (CW). The study was analyzed, using a one- and two-way ANOVA. RESULTS: Postexercise forced expiratory volume in the first second (FEV1) and maximal mid-expiratory flow (MMEF) values as percent predicted (% pred) showed significant reductions over time (P < 0.001), significant differences among the four experimental conditions (P < 0.001) and a significant condition x time interaction (FEV1:P < 0.001, MMEF:P < 0.01). FEV1 was significantly lower for CC and WC, as compared with WW and CW at 5 and 10 min postexercise. The lowest postexercise values for FEV1 occurred in the CC and WC sessions (76% predicted in both). A similar pattern was obtained for MMEF. CONCLUSION: Facial cooling combined with either cold or warm air inhalation causes the greatest EIB, as compared with the isolated challenge with cold air inhalation. We suggest that vagal mechanisms play a major role in exercise and cold-induced bronchoconstriction.

Analysis of Variance↗
PubMed1999

The effect of tulobuterol tape on histamine-induced bronchoconstriction in conscious guinea pigs: long duration of action.

The objective of the present study was to determine the action duration of tulobuterol tape within a 24-hr period in conscious guinea pigs. The bronchoconstriction induced by histamine-inhalation was significantly inhibited by tulobuterol tape in comparison with its placebo tape 8 and 12 hr after binding, and the inhibitory rate was 50+/-11% and 35+/-13%, respectively. Twenty-four hours after binding, the inhibitory effect of tulobuterol tape gradually diminished, but the inhibitory rate was maintained at 30+/-14%. These results suggest that tulobuterol tape has a long lasting bronchodilatory action.

Administration, Cutaneous↗
PubMed1992

Single-dose effect of astemizole on bronchoconstriction induced by histamine in asthmatic subjects.

STUDY OBJECTIVE: Astemizole, administered for seven days to asthmatic subjects, had an effect of bronchoconstriction induced by inhaled histamine for a mean period of 42 days. This study evaluates whether a single dose of astemizole would have the same effect. SUBJECTS: Sixteen adult asthmatic subjects took part in the study. DESIGN: They first underwent three inhalation tests and skin prick tests with histamine on three different days. On the last day, a methacholine inhalation test was also performed. They subsequently received either a placebo or an active preparation of astemizole. The histamine inhalation test was repeated one day, two days, one week, and/or ten days after administering the drug. RESULTS: Overall, no significant change in mean PC20 or in the mean diameter of the skin reaction to histamine was observed. However, three out of the eight subjects (38 percent) receiving active and none receiving placebo medication showed significant increases in PC20 histamine (p = 0.05). This effect lasted for one to two days. CONCLUSIONS: We conclude that a single dose of 10 mg/ml of astemizole can have a significant effect on bronchial but not cutaneous reactivity to histamine. This effect is of short duration (one to two days).

Adult↗
PubMed1993

Exercise, regardless of induced bronchoconstriction or inspired air conditions, does not alter airway reactivity.

The effects of exercise on asthmatic airway caliber are well recognized. Only a few studies, however, evaluated the effects of prior exercise on asthmatic airway reactivity. Eight asthmatic children (ages 10 to 16 years; mean, 12) performed histamine inhalation tests on three occasions assigned in random order: (1) control; (2) 40 to 60 min after exercise (6 min ergometer cycling) done while breathing cold dry (CD) air (temperature = -13 degrees C, relative humidity = 0 percent); and (3) 40 to 60 min after exercise done while breathing warm humid (WH) air (temperature = 33 degrees C, relative humidity = 100 percent). While there was a marked exercise-induced bronchoconstriction (EIB) in the CD test with a postexercise fall in FEV1 of 39.2 +/- 8 percent (mean +/- SEM), there was no EIB in the WH test (4.6 +/- 2 percent). There was no difference, however, in the geometric mean histamine concentration required to produce a 20 percent fall in FEV1 (PC20) among the CD, WH, and control tests (0.52 mg/ml, 0.60 mg/ml, and 0.55 mg/ml, respectively). Airway reactivity in asthmatic children is not influenced by a prior exercise challenge, independent of the conditions of the inspired air during the exercise. Moreover, exercise per se, regardless of development of EIB, does not change the reactivity.

Adolescent↗