Publications
1584 results found
Kidney JC, Lotvall JO, Lei YH, et al., 1996, The effect of inhaled K+ channel openers on bronchoconstriction and airway microvascular leakage in anaesthetised guinea pigs, EUROPEAN JOURNAL OF PHARMACOLOGY, Vol: 296, Pages: 81-87, ISSN: 0014-2999
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- Citations: 10
Sakamoto T, Chung KF, 1996, Lack of a role for bradykinin in inhaled sodium metabisulphite-induced airway microvascular leakage in guinea-pigs, Inflammopharmacology, Vol: 4, Pages: 323-330, ISSN: 0925-4692
We have investigated the role of bradykinin in airway microvascular leakage and bronchoconstriction induced by inhaled sodium metabisulphite (MBS) in guinea pigs. A selective bradykinin B2 receptor antagonist, HOE 140 (D-Arg[Hyp3,Thi5,D-Tic7,Oic8]-bradykinin), was used because this drug has been shown to abolish the airway responses induced by bradykinin. Lung resistance (R(L)) was measured for 6 min after challenge with MBS, followed by measurement of extravasation of Evans Blue dye into airway tissues, used as an index of plasma exudation. Aerosolized MBS (40 and 80 mmol/L, 30 breaths) induced a significant increase in R(L) and leakage of dye in the trachea, main bronchi and intrapulmonary airways, whereas 20 mmol/L MBS caused these responses except for the dye leakage in the trachea and main bronchi. HOE 140 (100 nmol/kg iv) had no effect against these airway responses. We conclude that bradykinin-mediated mechanisms do not play a significant role in the acute airway effects induced by inhaled MBS.
Lane SJ, Lee TH, 1996, Mast cell effector mechanisms, ISSN: 0091-6749
Several lines of evidence support the central role of the cysteinyl leukotrienes in aspirin-sensitive asthma, although their cellular source is unknown. The two most likely cells are the mast cell and eosinophil. Compared with aspirin-tolerant patients with asthma, patients with aspirin-sensitive asthma have been found to have a greater infiltration of mast cells and eosinophils in bronchial biopsy samples, although proportions of activated eosinophils were similar. Findings that support the involvement of mast cells include elevated serum histamine and tryptase levels after aspirin challenge in sensitive subjects, in line with a decrease in lung function and increased histamine and leukotriene C4 levels in nasal secretions; release of high-molecular-weight neutrophil chemotactic factor into serum after challenge; and prevention of aspirin-induced bronchoconstriction by pretreatment with cromolyn sodium or nedocromil sodium. These agents are also effective in protecting against bronchoconstriction induced by hyperosmolar stimuli, a challenge that is not associated with increased leukotriene E4 responsiveness but that is followed by increased release of histamine and prostaglandin D2 into bronchoalveolar lavage fluid. Antihistamines are poorly effective at inhibiting aspirin-induced bronchoconstriction but have been shown to attenuate the bronchoconstrictor response to hyperosmolar challenge. The main effector mechanism in hyperosmolar-induced bronchoconstriction appears to be mast cell activation and histamine release. Copyright © 1996 by Mosby-Year Book, Inc.
Chung KF, 1996, Methods of assessing cough and antitussives in man, PULMONARY PHARMACOLOGY & THERAPEUTICS, Vol: 9, Pages: 373-377, ISSN: 0952-0600
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- Citations: 6
Lalloo UG, Barnes PJ, Chung KF, 1996, Pathophysiology and clinical presentations of cough, Journal of Allergy and Clinical Immunology, Vol: 98, ISSN: 0091-6749
The human cough reflex is still poorly understood, although it is known to occur independently of bronchoconstriction. Sensitization of the cough reflex is a unifying hypothesis for chronic dry cough in several conditions, including gastroesophageal acid reflux, angiotensin-converting enzyme inhibitor cough, and cough-variant asthma. The most common cause of chronic dry cough is a group of related conditions of chronic rhinitis, sinusitis, and postnasal drip. In these cases the cough reflex may be sensitized through an action of inflammatory mediators from the nasal mucosa on the airways or a reflex sensitization of airway sensory nerves. The association of cough with gastroesophageal reflux may occur through a local esophageal-tracheobronchial reflex. Angiotensin-converting enzyme inhibitor cough is a side effect of treatment in about 10% of patients; it probably results from inhibition of the degradation of kinins, particularly bradykinin, in the airway. Why some patients with asthma have cough as the principal feature of their disease is unclear. Tachykinins are probably involved in the mechanism of sensitization of the cough reflex, and the development of neuropeptide antagonists may open new research opportunities. A study that used ambulatory recording of cough in a group of subjects with asthma confirmed the presence of significant cough, the frequency of which did not correlate with lung function or diurnal variation in peak flow. This finding highlights the problem of cough in patients with asthma, a problem that probably has been underestimated in the past. Copyright © 1996 by Mosby-Year Book, Inc.
Chung KF, 1996, Effects of nedocromil sodium on airway neurogenic mechanisms, Journal of Allergy and Clinical Immunology, Vol: 98, ISSN: 0091-6749
Evidence shows that nedocromil sodium has a major inhibitory effect on sensory nerve activation. Animal models in which inhibitory effects have been demonstrated include bradykinin- or ovalbumin-induced plasma extravasation; cigarette smoke- or sulfur dioxide-induced bronchial hyperresponsiveness and increase in inflammatory cells in the airway; and bradykinin-induced airway vasodilatation and nasal mucosal edema. Nedocromil sodium has prevented the edema in human skin induced by substance P and neurokinin A, and, in the isolated rabbit trachea, has prevented substance P-induced potentiation of cholinergic neural responses at preganglionic (but not postganglionic) sites. In vitro, the drug also has inhibited nonadrenergic noncholinergic bronchoconstriction in guinea pig bronchi. Although a protective effect against citric acid-induced cough in the dog has been reported, no data are available from models of enhanced cough reflex, such as that in asthma. Inhibition of sensory nerve activation and prevention of tachykinin release by nedocromil sodium probably contribute to its beneficial effects in the treatment of asthma. Copyright © 1996 by Mosby-Year Book, Inc.
Adcock IM, Gilbey T, Gelder CM, et al., 1996, Glucocorticoid receptor localization in normal and asthmatic lung, American Journal of Respiratory and Critical Care Medicine, Vol: 154, Pages: 771-782, ISSN: 1073-449X
The localization and distribution of the human glucocorticoid receptor (GR) mRNA and protein was investigated in human lung obtained from transplant donors and recipients by in situ hybridization, RNA blot analysis, immunolocalization, and Western analysis. Subjects were either nonasthmatic or had mild asthma requiring only β2-agonists. No difference in amount of GR mRNA was found in total RNA isolated from nonasthmatic or asthmatic donor lung. In situ hybridization showed the highest concentration of GR mRNA in the alveolar walls and vascular endothelium and smooth muscle, with lesser amounts in the airway epithelium and smooth muscle. There was no change in the level or sites of expression of GR mRNA between normal and asthmatic subjects. Immunolocalization of GR confirmed the in situ hybridization data. There was no change in the level or sites of expression of GR, in either the lung or airway, between normal and asthmatic subjects. Immunolocalization of GR in bronchial biopsies from two normal and asthmatic subjects confirmed the localization and distribution of GR. Western analysis and mobility shift assays confirmed no differences in GR levels between the two subject groups. The localization of GR mRNA and protein to specific cell types within lung and airway will make it possible to study the cellular targets of glucocorticoid therapy in inflammatory lung diseases such as asthma.
Yates DH, O'Connor BJ, Yilmaz G, et al., 1996, Erratum: Effect of acute and chronic inhaled furosemide on bronchial hyperresponsiveness in mild asthma (American Journal of Respiratory and Critical Care Medicine (1995) 152 (1170-1174)), American Journal of Respiratory and Critical Care Medicine, Vol: 153, ISSN: 1073-449X
Kharitonov SA, Chung KF, Evans D, et al., 1996, Increased exhaled nitric oxide in asthma is mainly derived from the lower respiratory tract, American Journal of Respiratory and Critical Care Medicine, Vol: 153, Pages: 1773-1780, ISSN: 1073-449X
Nitric oxide (NO) is detectable in the exhaled air of human subjects, and its concentration is increased in patients with asthma. We have investigated the origin of the increase in exhaled NO in asthmatic patients by using different expiratory maneuvers and by direct sampling from the upper and lower respiratory tracts. Exhaled NO was measured by a chemiluminescence analyzer. Concentrations of NO measured during expiration against the resistance of the analyzer with exhaled flow of 1 L/min, were 78 ± 3 ppb in normal subjects (n = 46) and significantly elevated in patients with asthma (301 ± 26 ppb, n = 30, p < 0.001). Values of exhaled NO were lower when measured during unobstructed expiration with a flow of 5 L/min with sampling from a side-arm (7 ± 1 ppb), but again were elevated in patients with asthma (46 ± 6 ppb, p < 0.001). Breath-holding for 20 s resulted in an initial peak of NO, but end-expiration values similar to the unobstructed expiration. The concentration of NO in the nose was considerably greater than in expired air (996 ± 39 ppb) and was elevated in patients with asthma (1,390 ± 71 ppb, p < 0.002). Direct sampling from trachea and right middle lobe bronchus via a fiberoptic bronchoscope gave similar values in five normal and 15 asthmatic subjects to the values recorded during unobstructed expiration, and there was a good correlation between values in expired air and direct sampling (trachea r = 0.91, right middle lobe r = 0.87, p < 0.001). We conclude that exhaled NO measured in an unobstructed breath reflects concentrations in the lower respiratory tract, but that breath-holding or expiration against resistance is contaminated by residual NO derived from the upper respiratory tract. We also provide evidence that the elevated levels of exhaled NO in asthmatic patients are derived predominantly from the lower respiratory tract.
Haczku A, MacAry P, Huang D, et al., 1996, CD4+ but not CD8+ T cells transfer allergic airway hyperresponsiveness (AHR) in BN-rats., Publisher: MOSBY-YEAR BOOK INC, Pages: 464-464, ISSN: 0091-6749
YATES DH, OCONNOR BJ, YILMAZ G, et al., 1995, EFFECT OF ACUTE AND CHRONIC INHALED FUROSEMIDE ON BRONCHIAL HYPERRESPONSIVENESS IN MILD ASTHMA, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 152, Pages: 2173-2175, ISSN: 1073-449X
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- Citations: 13
CAMBREY AD, KWON OJ, GRAY AJ, et al., 1995, INSULIN-LIKE GROWTH-FACTOR-I IS A MAJOR FIBROBLAST MITOGEN PRODUCED BY PRIMARY CULTURES OF HUMAN AIRWAY EPITHELIAL-CELLS, CLINICAL SCIENCE, Vol: 89, Pages: 611-617, ISSN: 0143-5221
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- Citations: 50
BERKMAN N, JOHN M, ROESEMS G, et al., 1995, INHIBITION OF MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA EXPRESSION BY IL-10 - DIFFERENTIAL SENSITIVITIES IN HUMAN BLOOD MONOCYTES AND ALVEOLAR MACROPHAGES, JOURNAL OF IMMUNOLOGY, Vol: 155, Pages: 4412-4418, ISSN: 0022-1767
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- Citations: 126
XU WB, HADDAD EB, TSUKAGOSHI H, et al., 1995, INDUCTION OF MACROPHAGE INFLAMMATORY PROTEIN-2 GENE-EXPRESSION BY INTERLEUKIN-1-BETA IN RAT LUNG, THORAX, Vol: 50, Pages: 1136-1140, ISSN: 0040-6376
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- Citations: 24
Haddad EB, Liu SF, Salmon M, et al., 1995, Expression of inducible nitric oxide synthase mRNA in Brown Norway rats exposed to ozone: effect of dexamethasone., Eur J Pharmacol, Vol: 293, Pages: 287-290, ISSN: 0014-2999
We studied the effects of ozone exposure and dexamethasone on inducible nitric synthase (iNOS) gene expression in Brown Norway rats in vivo. Using a murine iNOS cDNA probe, we detected a 4.4 kb iNOS mRNA by Northern analysis in rat lung. The iNOS signal was weak in control lungs, but increased in lungs exposed to ozone (3 ppm, 6 h). Ozone-induced iNOS mRNA expression was time-dependent, with maximal expression at 2 h, declining by 8 h and increasing again at 24 h postexposure. Dexamethasone significantly reduced the iNOS mRNA expression in the lungs of both controls and ozone-exposed rats. These results demonstrate that ozone inhalation induces iNOS expression in vivo, thus providing evidence at the molecular level for the possible involvement of nitric oxide generation in ozone-induced pulmonary inflammation or lung damage.
HADDAD EB, LIU SF, SALMON M, et al., 1995, EXPRESSION OF INDUCIBLE NITRIC-OXIDE SYNTHASE MESSENGER-RNA IN BROWN-NORWAY RATS EXPOSED TO OZONE - EFFECT OF DEXAMETHASONE, EUROPEAN JOURNAL OF PHARMACOLOGY-ENVIRONMENTAL TOXICOLOGY AND PHARMACOLOGY SECTION, Vol: 293, Pages: 287-290, ISSN: 0926-6917
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- Citations: 37
Yates DH, Sussman HS, Shaw MJ, et al., 1995, Regular formoterol treatment in mild asthma. Effect on bronchial responsiveness during and after treatment., Am J Respir Crit Care Med, Vol: 152, Pages: 1170-1174, ISSN: 1073-449X
Regular beta 2-adrenoceptor agonist therapy may lead to a rebound increase in bronchial responsiveness on discontinuation of therapy and a reduction in bronchoprotective effects. Formoterol, a long-acting beta 2-agonist, is effective in single doses in the prevention of methacholine-induced bronchoconstriction. In a double-blind, placebo-controlled cross-over study, we examined the effect of an inhaled long-acting beta 2-adrenoceptor agonist, formoterol (24 micrograms twice a day) for 2 wk on airway function and responsiveness in 17 subjects with mild asthma (mean age, 26.3 +/- 1.4 yr) who were not taking inhaled glucocorticosteroids. FEV1 and the provocative concentration of methacholine causing a 20% fall in FEV1 (PC20) were measured at 36, 60, and 108 h and at 2 wk after the last dose of regular treatment. In addition, PC20 was measured 12 h after the first and the last dose of formoterol and placebo. PC20 values at 36, 60, and 108 h and at 2 wk after formoterol treatment cessation were not significantly different from those after placebo. Mean FEV1 was 3.44 +/- 0.18 L after placebo compared with 3.79 +/- 0.20 L after formoterol (p < 0.001) 12 h after the first dose, and mean PC20 was 0.53 (GSEM 1.4) mg/ml after placebo compared with 2.0 (GSEM 1.4) mg/ml after formoterol (p < 0.001). After 2 wk of regular treatment, mean FEV1 at 12 h after the final dose of formoterol fell to 3.51 +/- 0.23 L compared with 3.41 +/- 0.18 L after the final dose of placebo (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
YATES DH, SUSSMAN HS, SHAW MJ, et al., 1995, REGULAR FORMOTEROL TREATMENT IN MILD ASTHMA - EFFECT ON BRONCHIAL RESPONSIVENESS DURING AND AFTER TREATMENT, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 152, Pages: 1170-1174, ISSN: 1073-449X
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- Citations: 100
LALLOO UG, FOX AJ, BELVISI MG, et al., 1995, CAPSAZEPINE INHIBITS COUGH INDUCED BY CAPSAICIN AND CITRIC-ACID BUT NOT BY HYPERTONIC SALINE IN GUINEA-PIGS, JOURNAL OF APPLIED PHYSIOLOGY, Vol: 79, Pages: 1082-1087, ISSN: 8750-7587
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- Citations: 156
BERKMAN N, JOSE PJ, WILLIAMS TJ, et al., 1995, CORTICOSTEROID INHIBITION OF MACROPHAGE INFLAMMATORY PROTEIN-1-ALPHA IN HUMAN MONOCYTES AND ALVEOLAR MACROPHAGES, AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY, Vol: 269, Pages: L443-L452, ISSN: 1040-0605
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- Citations: 39
HACZKU A, CHUNG KF, SUN J, et al., 1995, AIRWAY HYPERRESPONSIVENESS, ELEVATION OF SERUM-SPECIFIC IGE AND ACTIVATION OF T-CELLS FOLLOWING ALLERGEN EXPOSURE IN SENSITIZED BROWN-NORWAY RATS, IMMUNOLOGY, Vol: 85, Pages: 598-603, ISSN: 0019-2805
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- Citations: 53
SUN J, SAKAMOTO T, CHUNG KF, 1995, EFFECTS OF SODIUM METABISULFITE ON GUINEA-PIG CONTRACTILE AIRWAY SMOOTH-MUSCLE RESPONSES IN-VITRO, THORAX, Vol: 50, Pages: 875-879, ISSN: 0040-6376
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- Citations: 10
HACZKU A, MOQBEL R, JACOBSON M, et al., 1995, T-CELLS SUBSETS AND ACTIVATION IN BRONCHIAL-MUCOSA OF SENSITIZED BROWN-NORWAY RATS AFTER SINGLE ALLERGEN EXPOSURE, IMMUNOLOGY, Vol: 85, Pages: 591-597, ISSN: 0019-2805
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- Citations: 53
CHUNG KF, 1995, LEUKOTRIENE RECEPTOR ANTAGONISTS AND BIOSYNTHESIS INHIBITORS - POTENTIAL BREAKTHROUGH IN ASTHMA THERAPY, EUROPEAN RESPIRATORY JOURNAL, Vol: 8, Pages: 1203-1213, ISSN: 0903-1936
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- Citations: 63
MUNYARD P, CHUNG KF, BUSH A, 1995, INHALED FRUSEMIDE AND EXERCISE-INDUCED BRONCHOCONSTRICTION IN CHILDREN WITH ASTHMA, THORAX, Vol: 50, Pages: 677-679, ISSN: 0040-6376
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- Citations: 12
KIDNEY J, DOMINGUEZ M, TAYLOR PM, et al., 1995, IMMUNOMODULATION BY THEOPHYLLINE IN ASTHMA, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 151, Pages: 1907-1914, ISSN: 1073-449X
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- Citations: 203
Kidney J, Dominguez M, Taylor PM, et al., 1995, Immunomodulation by theophylline in asthma. Demonstration by withdrawal of therapy., Am J Respir Crit Care Med, Vol: 151, Pages: 1907-1914, ISSN: 1073-449X
Theophylline is the most widely used anti-asthma drug worldwide and is classified as a bronchodilator, although there is increasing evidence that it may have immunomodulatory effects. We have investigated the effects of theophylline withdrawal under placebo control in 27 asthmatic patients (25 to 70 yr) treated with long-term theophylline who were also treated with high dose inhaled corticosteroids. We measured asthma symptoms (diary card), lung function (spirometry and home records of peak expiratory flow), and peripheral leukocyte populations using dual color flow cytometry. In eight of these patients, we examined fiberoptic bronchial biopsies by immunocytochemistry. We also studied peripheral blood lymphocytes in eight asthmatic patients who have never received theophylline. Mean steady state plasma theophylline concentrations during theophylline therapy were 8.6 +/- 0.9 mg/L. Theophylline withdrawal was associated with a significant increase in asthma symptoms, particularly at night, and a fall in spirometry and morning peak flow. This was accompanied by a significant fall in peripheral blood monocytes (CD14+, activated CD4+ T-lymphocytes (CD4+/CD25+) and activated CD8+ T-cells (CD8+/HLA-DR+) in patients with a plasma theophylline > 5 mg/L. The lymphocyte populations in theophylline-naive patients were similar to those found after theophylline withdrawal. Bronchial biopsies showed a mirror image of the peripheral blood with an increase in CD4+ and CD8+ lymphocytes in the airway. Chronic treatment with theophylline, even at low plasma concentrations, controls asthma symptoms and has effects on T-lymphocyte populations in the peripheral blood which are the inverse of those observed in the airways.(ABSTRACT TRUNCATED AT 250 WORDS)
TSUKAGOSHI H, HADDAD EB, BARNES PJ, et al., 1995, BRADYKININ RECEPTOR SUBTYPES IN RAT LUNG - EFFECT OF INTERLEUKIN-1-BETA, JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS, Vol: 273, Pages: 1257-1263, ISSN: 0022-3565
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- Citations: 8
ROCA J, FELEZ MA, CHUNG KF, et al., 1995, SALBUTAMOL INHIBITS PULMONARY EFFECTS OF PLATELET-ACTIVATING-FACTOR IN MAN, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 151, Pages: 1740-1744, ISSN: 1073-449X
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- Citations: 19
KUITERT LM, ANGUS RM, BARNES NC, et al., 1995, EFFECT OF A NOVEL POTENT PLATELET-ACTIVATING-FACTOR ANTAGONIST, MODIPAFANT, IN CLINICAL ASTHMA, AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 151, Pages: 1331-1335, ISSN: 1073-449X
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- Citations: 60
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