Document Detail

Prostaglandin I2 enhances cough reflex sensitivity to capsaicin in the asthmatic airway.
Jump to Full Text
MedLine Citation:
PMID:  17222337     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Inflammatory mediators are involved in the pathogenesis of airway inflammation, but the role of prostaglandin I2 (PGI2) remains obscure. This study was designed to investigate the role of PGI2 in cough reflex sensitivity of the asthmatic airway, which is characterized by chronic eosinophilic airway inflammation. The effect of beraprost, a chemically and biologically stable analogue of PGI2, on cough response to inhaled capsaicin was examined in 21 patients with stable asthma in a randomized, placebo-controlled cross over study. Capsaicin cough threshold, defined as the lowest concentration of capsaicin eliciting five or more coughs, was measured as an index of airway cough reflex sensitivity. The cough threshold was significantly (p < 0.05) decreased after two weeks of treatment with beraprost [17.8 (GSEM 1.20) microM] compared with placebo [30.3 (GSEM 1.21) microM]. PGI2 increases cough reflex sensitivity of the asthmatic airway, suggesting that inhibition of PGI2 may be a novel therapeutic option for patients with asthma, especially cough predominant asthma.
Yoshihisa Ishiura; Masaki Fujimura; Kouichi Nobata; Yoshitaka Oribe; Miki Abo; Shigeharu Myou
Related Documents :
14578217 - Airway inflammation after cessation of exposure to agents causing occupational asthma.
6406587 - Neutrophil chemotactic activity in milk-induced asthma.
2117187 - Natural history of obstructive airways disease and hypoxia: implications for therapy.
17289447 - The i.v. infusion of mannitol decreases airway responsiveness to methacholine in asthma.
17874697 - Behavioral intervention, exercise, and nutrition education to improve health and fitnes...
17228987 - Understanding exercise behavior among korean adults: a test of the transtheoretical model.
Publication Detail:
Type:  Journal Article     Date:  2007-01-12
Journal Detail:
Title:  Cough (London, England)     Volume:  3     ISSN:  1745-9974     ISO Abbreviation:  -     Publication Date:  2007  
Date Detail:
Created Date:  2007-01-24     Completed Date:  2007-07-23     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  101245793     Medline TA:  Cough     Country:  England    
Other Details:
Languages:  eng     Pagination:  2     Citation Subset:  -    
The Department of Internal Medicine, Toyama City Hospital, Toyama, Japan.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Full Text
Journal Information
Journal ID (nlm-ta): Cough
ISSN: 1745-9974
Publisher: BioMed Central, London
Article Information
Download PDF
Copyright ? 2007 Ishiura et al; licensee BioMed Central Ltd.
open-access: This is an Open Access article distributed under the terms of the Creative Commons Attribution License (), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Received Day: 16 Month: 11 Year: 2005
Accepted Day: 12 Month: 1 Year: 2007
collection publication date: Year: 2007
Electronic publication date: Day: 12 Month: 1 Year: 2007
Volume: 3First Page: 2 Last Page: 2
ID: 1781075
Publisher Id: 1745-9974-3-2
PubMed Id: 17222337
DOI: 10.1186/1745-9974-3-2

Prostaglandin I2 enhances cough reflex sensitivity to capsaicin in the asthmatic airway
Yoshihisa Ishiura1 Email:
Masaki Fujimura2 Email:
Kouichi Nobata2 Email:
Yoshitaka Oribe1 Email:
Miki Abo1 Email:
Shigeharu Myou2 Email:
1The Department of Internal Medicine, Toyama City Hospital, Toyama, Japan
2Respiratory Medicine, Cellular Transplantation Biology, Kanazawa University Graduate School of Medicine, Kanazawa, Japan


Chronic cough is one of the commonest respiratory symptoms. Cough has been considered to be a defense mechanism of the airway to remove irritant particles or excess mucus, whereas non-productive cough, which is not associated with the clearance of the tracheobronchial mucus, may occur via increased cough reflex sensitivity. Inflammatory mediators such as prostaglandins may adjust the cough reflex sensitivity. However, little is known about how cough reflex sensitivity is influenced by airway inflammatory processes. Although our previous study has clearly shown that arachidonate cyclooxygenase products can modulate airway cough reflex sensitivity to inhaled capsaicin [1], the effects of other mediators remains unknown.

It has been recognized that prostaglandin I2 (PGI2, prostacyclin) is the most abundant prostanoid generated on IgE-dependent challenge of human lung tissue in vitro [2,3]. Others reported that alveolar macrophages are able to synthesize large amount of PGI2 [4]. These findings indicate that PGI2 may play some role in the asthmatic airway and can affect airway cough reflex sensitivity. This study was conducted to elucidate this hypothesis. We investigated the effect of oral administration of beraprost, a chemically and biologically stable analog of PGI2 {sodium (?)-4[(1R, 2R, 3aS, 8bS)-1, 2, 3a, 8b-tetrahydro-2-hydroxyl 2[(3S, 4RS)-3-hydroxy-4-methyl-oct-6-yne-(E)-l-enyl]-5-cyclopenta [b] benzofuranyl] butyrate}, on cough reflex sensitivity to inhaled capsaicin in patients with stable asthma [5].

Subjects and Methods

Twenty-one patients with bronchial asthma (12 males and 9 females) with a mean age of 73.2 ? 1.5 (? SEM) (range 54?83) yrs participated in this study. All patients were lifetime nonsmokers or ex-smokers with no history of viral infection for at least 4 weeks prior to the study. Characteristics of individual patients are shown in Table 1. Informed consent was obtained from all subjects. This study was approved by the Ethics Committee of our hospital.

Each asthmatic patient satisfied the American Thoracic Society definition of asthma, with symptoms of episodic wheezing, cough, and shortness of breath responding to bronchodilators, and reversible airflow obstruction documented on at least one previous pulmonary function study [6]. Reversibility was defined as greater than 12 % and 200 ml increase in the forced expiratory volume in one second (FEV1) following a bronchodilator inhalation (Table 1). All patients had bronchial hyperresponsiveness as shown in Table 1. Classification of asthma severity was defined according to Global Strategy for Asthma Management and Prevention. Patients with atopy were recognized as having a hereditary tendency to produce IgE antibodies against common environmental allergens [7]. This study was carried out when symptoms were mild and stable, while patients were taking oral theophylline, oral (short-acting clenbuterol) and/or aerosol ?2-agonists (short-acting procaterol), inhaled steroids (beclomethasone dipropionate), inhaled anti-cholinergic agents (oxitropium bromide) and/or mucolytic agents (carbocysteine) according to previous reports [8-10]. They had not received oral steroids for at least eight weeks.

Assessment of cough reflex sensitivity to inhaled capsaicin

Cough reflex sensitivity was assessed by capsaicin provocation test [11]. Capsaicin (30.5 mg) was dissolved in Tween 80 (1 mL) and ethanol (1 mL) and then dissolved in physiological saline (8 mL) to make a stock solution of 1 ? 10-2 M, which was stored at -20?C. This solution was diluted with physiological saline to make solutions starting at a concentration of 0.49 ?M and increasing it by doubling concentrations up to 1000 ?M. Each subject inhaled a control solution of physiological saline followed by progressively increasing concentrations of the capsaicin solution. Solutions were inhaled for 15 s every 60 s, by tidal mouth-breathing wearing a noseclip from a Bennett Twin nebulizer (3012-60 cc, Puritan-Bennett Co., Carlsbad, California, USA). Increasing concentrations were inhaled until five or more coughs were elicited. The nebulizer output was 0.21 mL/min. The number of capsaicin-induced coughs was counted by a blinded medical technician in our pulmonary function laboratory. The cough threshold was defined as the lowest concentration of capsaicin that elicited five or more coughs.

Study protocol (Figure 1)

The medication was stopped at 9.00 p.m. on the previous day to allow a washout time of 12 h or more before the measurement of cough threshold to inhaled capsaicin at 10.00 a.m. on each test day to reduce the diurnal variability of the cough response.

Each patient attended 4 times separated by 2 weeks, at the same time each day. Control measurement of capsaicin cough threshold was carried out 2 weeks before initiation of the first treatment (run-in). Two weeks treatment with beraprost sodium or placebo was performed separated by a two-week washout period in a randomized, cross-over fashion. Two beraprost sodium tablets (40 ?g) and their placebo were taken orally three times a day for 14 days and at 8.00 a.m. on the test day. FEV1 was measured on a dry wedge spirometer (Transfer Test, P.K. Morgan Ltd., UK) before capsaicin challenge to assess the bronchoactive effect of the treatment regimens. Serum total IgE levels and the number of peripheral eosinophils were measured to assess anti-allergic effect of the test drugs.

Data analysis

Capsaicin cough threshold values were expressed as geometric mean with geometric standard error of the mean (GSEM). Forced vital capacity (FVC), FEV1 and maximal mid expiratory flow (MMF) were shown as arithmetic mean values ? SEM. The FVC values, the FEV1 values and the MMF values were compared between each pair of the four groups (run-in, washout, beraprost sodium and placebo) by the Wilcoxon signed-ranks test. A p-value of 0.05 or less was taken as significant.


Cough threshold to inhaled capsaicin before each treatment (run-in, washout) and after treatment with beraprost and placebo are shown in Figure 2. Geometric mean values for the cough threshold were 29.5 (GSEM 1.17) ?M in the run-in period, 26.5 (GSEM 1.18) ?M in the washout period, 17.8 (GSEM 1.20) ?M after beraprost treatment and 30.3 (GSEM 1.21) ?M after placebo treatment. The cough threshold after the beraprost treatment was significantly (p < 0.05) lower than the value after the placebo treatment. FVC, FEV1 or MMF value was not significantly different between run-in period, washout period, beraprost treatment and placebo treatment as shown in Table 2.

Figure 3 and figure 4 show the changes in serum IgE and peripheral blood eosinophils, respectively. Treatment with beraprost did not affect the IgE production or peripheral blood eosinophil count.


The present study showed that two-week treatment with a stable PGI2 analogue, beraprost, decreased the cough threshold to inhaled capsaicin in asthmatic patients. No difference could be found in the baseline pulmonary function, IgE production or peripheral eosinophil count between beraprost and placebo treatments. These findings suggest that PGI2 enhances the cough reflex sensitivity in the asthmatic airway.

Cough is one of the main symptoms of bronchial asthma which can profoundly and adversely affect the quality of patient's lives and social activities, whereas the mechanisms underlying the cough remain obscure. Previous researchers [12] indicated that cough receptors are stimulated by local bronchoconstriction. This finding may be one of the causes of cough in bronchial asthma. However, recent studies about cough variant asthma (CVA) revealed normal baseline pulmonary function and mild bronchial hyperresponsiveness [13,14]. Our previous study has also demonstrated that inhaled procaterol in a dose sufficient to produce bronchodilation has no effect on airway cough receptor sensitivity in asthma [15]. O'Connell and colleagues have reported that cough reflex sensitivity is increased in some asthmatic patients suffering from daily coughing and recovers to normal range after relief of the cough on treatment [16]. These findings suggest that cough reflex hypersensitivity is another mechanism of chronic non-productive cough in asthma, in addition to cough receptor stimulation by local bronchoconstriction [12].

It has been revealed that inflammatory mediators such as arachidonate metabolites play major roles in the pathogenesis of bronchial asthma, however, the relationship between inflammatory mediators and airway cough reflex sensitivity remains obscure. Some studies indicated that some inflammatory mediators might modulate the sensitivity of cough reflex [1,17]. We showed that intrinsic thromboxane A2 (TxA2) is a possible modulator augmenting both airway cough reflex sensitivity and bronchial responsiveness while it does not have bronchoconstricting effect in stable asthmatics [1,18,19]. Other researchers reported that prostaglandin F2? (PGF2?) enhances airway cough reflex sensitivity with bronchoconstricting effect [2,20]. It has been also shown that inhaled prostaglandin E2 (PGE2), which acts as a bronchodilator, enhances cough reflex sensitivity [20,21]. Although cysteinyl leukotrienes (cLTs) play an important role in bronchomotor tone of the asthmatic airway, their role in cough reflex sensitivity is controversial [19,22]. These findings indicate that arachidonate metabolites including prostaglandins may have variable roles in the local control of the cough reflex with no relation to bronchoconstriction.

It has been known that PGI2 is the most abundant prostanoid generated on IgE-dependent challenge of human lung tissue in vitro [2,3]. Others reported that alveolar macrophages are able to synthesize a large amount of PGI2 [4]. These findings imply that PGI2 plays some role in asthmatic airway. Although PGI2 causes relaxation of isolated precontracted human bronchus [23], its clinical effect is limited: short-term protection against immediate bronchoconstriction provoked by exercise [24], and nebulized distilled water [24] but not by allergen [25] or aspirin [26]. Therefore, the exact role of PGI2 in asthmatic airway remains obscure. Hardy et al. reported an irritative effect of single inhalation of PGI2 on human airways [27], but influence of repeated administration has not been studied. Szczeklik and their colleagues also reported that four out of twelve asthmatic patients complained of coughing during PGI2 inhalation [28]. However, these previous reports have not investigated the change of cough reflex sensitivity. Thus the exact role of PGI2 in airway cough reflex sensitivity also remains unknown. We observed that some patients complained of coughing on treatment with beraprost but none did with placebo. The implication of this study is that PGI2 may be involved in the pathogenesis of cough reflex sensitivity rather than bronchodilation and it may explain the role of PGI2 in the asthmatic airway which has been unknown so far.

Overall, our data support the conclusion that inhibition of PGI2 formation or action may be a novel treatment for chronic non-productive cough in asthmatic airway, especially in cough variant asthma or cough predominant asthma with normal baseline pulmonary function. This is the first report demonstrating the role of PGI2 in cough reflex sensitivity in the asthmatic airway. Further studies may be required to elucidate the role of PGI2 in other eosinophilic bronchial disorders presenting with non-productive cough with normal baseline pulmonary functions [29-31].


cLT = cysteinyl leukotriene; CVA = cough variant asthma; FEV1 = forced expiratory volume in one second; FVC = forced vital capacity; GSEM = geometric standard error of the mean; PGE2 = prostaglandin E2; PGF2? = prostaglandin F2?; PGI2 = prostaglandin I2; MMF = maximal mid expiratory flow; TxA2 = thromboxane A2.


This study was supported in part by a grant-in-aid for Scientific Research from the Ministry of Education, Science and Culture (17607003) by the Japanese Government.

Fujimura M,Kamio Y,Kasahara K,Bando T,Hashimoto T,Matsuda T. Prostanoids and cough response to capsaicin in asthma and chronic bronchitisEur Respir J 1995;8:1499–1505. [pmid: 8575575]
Horton EW. Prostaglandins and smooth muscleBr Med Bull 1979;35:295–300. [pmid: 575306]
Schulman ES,Adkinson NF,Newball HH. Cyclooxygenase metabolites in human lung anaphylaxis. Airways vs. parenchymaJ Appl Physiol 1982;53:589–595. [pmid: 6813301]
Hsueh W,Kuhn GIII,Needleman P. Relationship of prostaglandin secretion by rabbit alveolar macrophages to phagocytosis and lysosomal enzyme releaseBiochem J 1979;184:345–54. [pmid: 534533]
Akiba T,Miyazaki M,Toda N. Vasodilator actions of TKR-100, a new prostaglandin I2 analogueBr J Pharmacol 1986;89:703–711. [pmid: 3101928]
American Thoracic SocietyStandards for the diagnosis and care of patients with chronic obstructive pulmonary disease (COPD) and asthmaAm Rev Respir Dis 1987;136:225–244. [pmid: 3605835]
Kay AB. Allergy and allergic diseasesN Engl J Med 2001;344:30–37. [pmid: 11136958] [doi: 10.1056/NEJM200101043440106]
Fujimura M,Kamio Y,Hashimoto T,Matsuda T. Cough receptor sensitivity and bronchial responsiveness in patients with only chronic nonproductive cough: in view of effect of bronchodilator therapyJ Asthma 1994;31:463–72. [pmid: 7961323]
Boner AL,Vallone G,Brighenti C,Schiassi M,Miglioranzi P,Richelli C. Comparison of the protective effect and duration of action of orally administered clenbuterol and salbutamol on exercise-induced asthma in childrenPediatr Pulmonol 1988;4:197–200. [pmid: 3393382]
Ishiura Y,Fujimura M,Yamamori C,Nobata K,Myou S,Kurashima K,Michishita Y,Takegoshi T. Effect of carbocysteine on cough reflex to capsaicin in asthmatic patientsBr J Clin Pharmacol 2003;55:504–10. [pmid: 12814442] [doi: 10.1046/j.1365-2125.2003.01788.x]
Fujimura M,Sakamoto S,Kamio Y,Matsuda T. Effects of methacholine-induced bronchoconstriction and procaterol-induced bronchodilation on cough receptor sensitivity to inhaled capsaicin and tartaric acidThorax 1992;47:441–45. [pmid: 1386691]
Salem H,Aviado DM. Antitussive drugsAm J Med Sci 1964;247:585–600. [pmid: 14158494]
Corrao WM,Braman SS,Irwin RS. Chronic cough as the sole presenting manifestation of bronchial asthmaN Engl J Med 1979;300:633–637. [pmid: 763286]
Koh YY,Chae SA,Min KU. Cough variant asthma is associated with a higher wheezing threshold than classic asthmaClin Exp Allergy 1993;23:696–701. [pmid: 8221272] [doi: 10.1111/j.1365-2222.1993.tb01796.x]
Fujimura M,Sakamoto S,Kamio Y,Bando T,Kurashima K,Matsuda T. Effect of inhaled procaterol on cough receptor sensitivity in patients with asthma or chronic bronchitis and in normal subjectsThorax 1993;48:615–618. [pmid: 8346491]
O'Connell F,Thomas VE,Pride NB,Fuller RW. Capsaicin cough sensitivity decreases with successful treatment of chronic coughAm J Respir Crit Care Med 1994;150:374–380. [pmid: 8049818]
Choudry NB,Fuller RW,Pride NB. Sensitivity of the human cough reflex: Effect of inflammtory mediators prostaglandin E2, bradykinin, and histamineAm Rev Respir Dis 1989;140:137–141. [pmid: 2751160]
Fujimura M,Sakamoto S,Saito M,Miyake Y,Matsuda T. Effect of a thromboxane A2 receptor antagonist (AA-2414) on bronchial hyperresponsiveness to methacholine in asthmatic subjectsJ Allergy Clin Immunol 1991;87:23–27. [pmid: 1825100] [doi: 10.1016/0091-6749(91)90208-6]
Fujimura M,Kamio Y,Hashimoto T,Matsuda T. Thromboxane A2 and sulfidopeptide leukotrienes in cough reflex in response to inhaled capsaicin in asthmatic subjectsJ Jpn Soc Bronchology 1998;20:4–10.
Stones R,Barnes PJ,Fuller RW. Contrasting effects of prostaglandins E2 and F2_ on sedisitivity of the human cough reflexJ Appl Physiol 1992;73:649–653. [pmid: 1399993]
Wasserman MA,Griffin RL,Marsalisi FB. Inhibition of bronchoconstriction by aerosols of prostaglandins E1 and E2J Pharmacol Exp Ther 1980;214:68–73. [pmid: 7391972]
Dicpinigaitis PV,Dobkin JB. Effect of zafirlukast on cough reflex sensitivity in asthmaticsJ Asthma 1999;36:265–70. [pmid: 10350223]
Gardiner PJ,Coller HO. Specific receptors for prostaglandins in airwaysProstaglandins 1980;19:819–841. [pmid: 6247749] [doi: 10.1016/0090-6980(80)90116-1]
Bianco S,Robuschi M,Ceserani R,Gandolfi C,Kambuff P. Prevention of specifically induced bronchoconstriction by PGI2 and 20-methyl-PGI2 in asthmatic patientsPharmacol Res Commun 1978;10:657–675. [pmid: 362433] [doi: 10.1016/S0031-6989(78)80009-5]
Bianco S,Robuschi M,Ceserani R,Gandolfi C. Effects of prostacyclin on aspecifically and specifically induced bronchoconstriction in asthmatic subjectsEur J Respir Dis 1980;S106:18–87.
Nizankowska E,Czerniawska-mysik ,Szczeklik A. Lack of effect of i.v. prostacyclin on aspirin induced asthmaEur J Respir Dis 1986;69:363–368. [pmid: 3539632]
Hardy C,Robinson C,Lewis RA,Tattersfield AE,Holgate ST. Airway and cardiovascular responses to inhaled prostacyclin in normal and asthmatic subjectsAm Rev Respir Dis 1985;131:18–21. [pmid: 2981491]
Szczeklik A,Gryglewski RJ,Nizankowska E,Nizankowski R,Musial J. Pulmonary and anti-platelet effects of intravenous and inhaled prostacyclin in manProstaglandins 1978;16:651–60. [doi: 10.1016/0090-6980(78)90001-1]
Gibson PG,Dolovich J,Denburg J,Ramsdale EH,Hargreave FE. Chronic cough: eosinophilic bronchitis without asthmaLancet 1989;1:1346–1348. [pmid: 2567371] [doi: 10.1016/S0140-6736(89)92801-8]
Fujimura M,Ogawa H,Yasui M,Matsuda T. Eosinophilic tracheobronchitis and airway cough hypersensitivity in chronic non-productive coughClin Exp Allergy 2000;30:41–47. [pmid: 10606929] [doi: 10.1046/j.1365-2222.2000.00698.x]
Brightling CE,Ward R,Goh KL,Wardlaw AJ,Pavord ID. Eosinophilic bronchitis is an important cause of chronic coughAm J Respir Crit Care Med 1999;160:406–410. [pmid: 10430705]


[Figure ID: F1]
Figure 1 

Study protocol.

[Figure ID: F2]
Figure 2 

Individual data of capsaicin cough threshold at run-in period, at washout period and on treatment with beraprost and placebo in patients with stable bronchial asthma. Each horizontal bar represents geometric mean value. Closed circles and open circles represent patients undergoing steroid inhalation therapy and patients without steroid inhalation therapy, respectively. P values: Wilcoxon signed-ranks test using logarithmically transformed values.

[Figure ID: F3]
Figure 3 

Individual data of serum IgE at run-in period, at washout period and on treatment with beraprost and placebo in patients with stable bronchial asthma. Each horizontal bar represents geometric mean value. Closed circles and open circles represent patients undergoing steroid inhalation therapy and patients without steroid inhalation therapy, respectively. P values: Wilcoxon signed-ranks test using logarithmically transformed values.

[Figure ID: F4]
Figure 4 

Individual data of peripheral blood eosinophils at run-in period, at washout period and on treatment with beraprost and placebo in patients with stable bronchial asthma. Each horizontal bar represents geometric mean value. P values: Wilcoxon signed-ranks test.

[TableWrap ID: T1] Table 1 

Clinical characteristics of patients

Patient number Age (yr) Sex Height (cm) Type Severity Total IgE in serum (IU/ml) Specific IgE in serum Complication of allergic disease PC20-FEV1 (mg/ml)* Bronchodilator response (%)** Treatment

BDP (?g/day) Theophylline (mg/day) Clenbuterol (?g/day) Carbocysteine (mg/day)
1 54 M 161 Int Moderate 420 - - 2.5 15.2 800 400 40 0
2 72 F 147 Ext Moderate 642 Mite, HD AR 0.31 31.5 800 400 0 0
3 70 M 161 Ext Mild 312 Mite, HD, Cedar - 0.08 20.2 0 600 0 0
4 71 F 140 Int Mild 17 - - 1.25 17.6 800 0 0 0
5 83 M 154 Ext Moderate 345 Mite, HD, Cedar - 5 17.1 800 400 40 1500
6 71 M 165 Ext Moderate 146 Mite, HD AR 1.25 15.6 0 0 40 0
7 77 F 144 Int Mild 51 - - 0.31 17.9 0 0 0 1500
8 71 M 155 Int Mild 42 - - 2.5 29.4 800 0 0 1500
9 80 M 152 Int Moderate 66 - - 1.25 39 800 0 0 0
10 75 M 162 Ext Mild 143 Candida - 2.5 14.1 800 0 0 0
11 80 F 145 Ext Mild 3 HD, Cedar - 0.08 37.1 800 0 0 0
12 63 F 154 Ext Moderate 77 Cedar AR 1.25 14.7 800 0 0 0
13 77 F 142 Int Mild 105 - - 5 17 0 400 20 0
14 70 M 155 Int Moderate 82 - - 0.31 15.4 800 0 0 1500
15 70 F 151 Ext Mild 467 Mite, HD - 2.5 20.4 800 400 40 0
16 72 F 150 Int Mild 57 - - 5 22.3 600 0 0 1500
17 81 M 163 Int Moderate 64 - - 0.31 33.4 800 600 40 1500
18 71 M 150 Int Moderate 107 - - 5 16.4 800 400 40 0
19 80 M 160 Int Mild 87 - - 2.5 29.5 0 400 0 0
20 68 M 167 Ext Mild 264 Cedar - 5 27 0 400 40 0
21 80 F 152 Int Mild 54 - - 2.5 17.3 0 400 0 0

Ext, extrinsic; Int. Intrinsic; HD, house dust; AR, allergic rhinitis; UR, urticaria; BDP, beclomethasone diproprionate inhalation.

* PC20-FEV1 shows concentration of inhaled methacholine causing a 20% fall in FEV1.

** Bronchodilator response means percent increase in forced expiratory volume in 1s (FEV1) from the baseline value after inhalation of 300 ?g of salbutamol sulfate.

All patients used inhaled ?2-agonists (salbutamol or procaterol) on demand.

[TableWrap ID: T2] Table 2 

Pulmonary function on beraprost and placebo treatments in patients with bronchial asthma

Run-in Placebo Washout Beraprost
FVC as % pred. (%) 96.8 ? 5.7 103.4 ? 3.3 104.4 ? 3.1 103.4 ? 3.4
FEV1 as% pred. (%) 90.9 ? 5.7 94.1 ? 5.5 93.0 ? 5.6 93.2 ? 5.6
MMF as% pred. (%) 50.7 ? 6.7 52.0 ? 6.0 50.1 ? 6.4 51.5 ? 6.4

Data are shown as standard error of the mean for FVC, FEV1 and MMF.

* p < 0.05 compared with each control value (Wilcoxon signed-ranks test).

Article Categories:
  • Research

Previous Document:  Transcriptional profiling of the LPS induced NF-kappaB response in macrophages.
Next Document:  Wnt/beta-catenin signaling is required for development of the exocrine pancreas.