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Biomedical subjects

H Magnussen

Publications and source records attributed to H Magnussen.

At least 217 records · Page 12Linked to original sources
PubMed1992

Influence of exercise-induced bronchoconstriction on refractoriness.

This study determined if the degree of exercise-induced refractoriness is determined by the degree of exercise-induced bronchoconstriction. In 12 patients with exercise-induced asthma (mean [SEM] age 27 [3] years) we performed 2 pairs of exercise challenges 45 min apart at different work loads on 2 days. Mean (SEM) total respiratory heat loss during low and high work loads was 3.4 (0.2) and 5.1 (0.4) kcal, respectively. After the first and second exercise challenge at low work loads, mean (SEM) SRaw increased by 107 (15) and 73 (16)% (n.s.), as compared to 361 (40) and 98 (25)% at high work loads (p less than 0.005). We found a correlation between the initial airways response and refractoriness (r = 0.58, p less than 0.005) and conclude that the degree of refractoriness after exercise-induced bronchoconstriction is in part dependent on the severity of exercise-induced bronchoconstriction.

Adult↗
PubMed1992

Formation of benzo[a]pyrene-DNA adducts in blood monocytes from lung cancer patients with a familial history of lung cancer.

The in vitro formation of benzo[a]pyrene-DNA adducts was determined in peripheral blood monocytes of 22 lung cancer patients with at least one first-degree relative with lung cancer and compared to results obtained in 30 healthy controls. In patients, the mean (SEM) adduct formation was 2.8 (0.3) fmol/micrograms DNA as compared to 2.1 (0.1) fmol/micrograms in controls (p less than 0.05), and it was independent of age and smoking habits. These findings support the hypothesis that carcinogen-DNA adduct formation may be one factor of a constitutionally enhanced lung cancer risk.

Adenocarcinoma↗
PubMed1992

Salmeterol protects against hyperventilation-induced bronchoconstriction over 12 hours.

To study the dose-response relationship of salmeterol for protection against a naturally occurring stimulus, isocapnic hyperventilation tests of cold air were done in 16 asthmatic patients. The subjects inhaled either 50 micrograms salmeterol, salbutamol 200 micrograms, or placebo in a double-blind, randomised, cross-over study. The FEV1 was measured prior to medication and the provocative ventilation (PV20) required to induce a 20% fall in FEV1 was calculated by linear interpolation from ventilation-response curves obtained 0.5, 4, 8, and 12 h after medication. Following salbutamol, the mean FEV1 were 4.11, 3.89, 3.58, and 3.55 l, with a significant difference from placebo up to 4 h. Following salmeterol, mean FEV1 values were 3.95, 4.10, 3.93, and 3.88 l, with a significant difference from placebo up to 12 h. The mean PV20FEV1 after salbutamol was 78.8, 58.5, 52.7, and 48.4 l.min-1, the 0.5 h value being significantly different from placebo. After salmeterol, the mean PV20FEV1 values were 84.6, 82.5, 67.8, and 65.8 l.min-1, with a significant difference from placebo up to 12 h. We conclude that, besides its long-lasting bronchodilating effect, salmeterol protects against hyperventilation-induced bronchoconstriction for at least 12 h.

Adult↗
PubMed1992

The protective effect of low-dose inhaled fenoterol against methacholine and exercise-induced bronchoconstriction in asthma: a dose-response study.

We compared in a randomized, double-blind study the protective effect of low doses of fenoterol on the airway response to exercise during cold air breathing and an inhalation challenge with methacholine. In six asymptomatic asthmatic persons (mean age, 20.3 years) exercise and methacholine challenges were performed under control conditions and 15 minutes after the inhalation from a metered-dose inhaler of either placebo or 30, 50, 100, and 200 micrograms fenoterol, resulting in 12 separate study sessions within a 3-week period. Airway response was determined by measuring specific airway resistance (sRaw). Exercise tests were standardized by maintaining a constant respiratory heat exchange, with an average (range) of 1.28 (1.15 to 1.45) kcal/min. Methacholine was inhaled at increasing doses until sRaw had doubled (PD100sRaw). Mean postexertional increase of sRaw (SD) after control conditions, placebo, and 30, 50, 100, and 200 micrograms fenoterol aerosol was 27.8 (6.9), 28.9 (10.0), 7.20 (2.7), 9.33 (3.8), 5.57 (2.3), and 5.28 (1.6) cm H2O.s. Fenoterol aerosol was equally effective at all doses administered, whereas methacholine-induced bronchoconstriction was attenuated in a dose-dependent manner. From these observations we suggest that low-dose fenoterol protects against bronchoconstriction induced by exercise, a naturally occurring stimulus reflecting airway hyperresponsiveness.

Adolescent↗
PubMed1992

Effects of a thromboxane-receptor antagonist, BAY u 3405, on prostaglandin D2- and exercise-induced bronchoconstriction.

In the pathogenesis of exercise-induced bronchoconstriction (EIB), prostaglandin D2 (PGD2) may play a role as a newly generated, mast cell-derived mediator. As the bronchoconstrictor effects of PGD2 are predominantly mediated via stimulation of thromboxane receptors in the lung, we studied a novel, orally effective, thromboxane-receptor antagonist, BAY u 3405, on EIB in 12 male subjects with mild asthma. On 4 study days, we determined, in a randomized, double-blind, placebo-controlled, crossover fashion, the effects of 20 mg of BAY u 3405 administered orally 1 hour before PGD2 and exercise challenges, respectively. Increasing dosages of PGD2 were inhaled to establish dose-response curves that allowed determination of the provocative concentration necessary to decrease FEV1 by at least 20% (PC20) and to increase specific airway resistance (SR(aw)) by 100% (PC100). EIB was measured as a maximal fall/increase in postexertional FEV1/SR(aw) after bicycle exercise and cold-air breathing. Prechallenge lung-function values were similar on all four occasions. BAY u 3405 did not elicit any effect on resting bronchial tone. After placebo, the geometric means (SD) of PC20 and PC100 were 0.0380 (2.6) and 0.0266 (2.4) mg/ml, increasing to 0.554 (5.9) and 0.143 (8.1) mg/ml after BAY u 3405 (p = 0.0002). Mean (SD) maximal postexertional decrease in FEV1 and increase in SR(aw) after placebo was 29.4% (16.4%) and 280% (135%), and after BAY u 3405, 31.4% (18.1%) and 379% (281%) (not significant). No clinically relevant BAY u 3405-related side effects were observed. From these results we conclude that BAY u 3405 is highly effective in attenuating PGD2-induced bronchoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Air↗
PubMed1992

Clinical evidence of systemic persistence of bacillus Calmette-Guerin: long-term pulmonary bacillus Calmette-Guerin infection after intravesical therapy for bladder cancer and subsequent cystectomy.

A patient with urothelial bladder carcinoma is reported who suffered from culture proved pulmonary bacillus Calmette-Guerin (BCG) infection 14 months after a single course of intravesical BCG and 11 months after subsequent radical cystectomy for progressive cancer. This unusual case raises the question of the ultimate fate of intravesically instilled BCG and the possible persistence of these mycobacteria in remote organs. Systemic spread and dormant survival at least in some cases are suggested, and therapeutic and diagnostic consequences are discussed.

Administration, Intravesical↗
PubMed1992

Low dose fenoterol aerosol protects against histamine-induced bronchoconstriction in mild asthmatics: a dose response study.

Sixteen subjects with mild stable asthma participated in a randomized double blind study on the effects of low dose fenoterol against histamine induced bronchoconstriction. Fenoterol aerosol at concentrations of 10, 50 and 200 micrograms and placebo were delivered at random through a metered dose inhaler as a single dose 30 min before histamine challenges on four separate occasions. Compared to placebo a fenoterol dose of 10 micrograms provided significant bronchodilatation (sRaw [s.d.] 8.3 [2.73] vs 6.3 [1.74] cm H2O* s [P less than 0.05]) and protection (PC100 sRaw [s.e.m.] 0.72 (1.31) vs 1.45 (1.39) mg/ml). The bronchodilatory and protective actions of fenoterol were more pronounced after the inhalation of 200 micrograms (P less than 0.05) with no difference between 10 and 50 micrograms fenoterol aerosol. The magnitude of bronchodilatation and protection was not correlated (r = 0.15). The results from this acute study may suggest that fenoterol at doses up to 20 times lower than routinely recommended may be an effective treatment in mild asthmatics.

Adult↗
PubMed1992

Effect of inhaled ipratropium bromide on the airway response to methacholine, histamine, and exercise in patients with mild bronchial asthma.

We studied the bronchodilator and protective potency of inhaled ipratropium bromide in 33 patients with mild bronchial asthma. Patients were divided into 3 groups with similar baseline lung function and similar degrees of bronchial hyperresponsiveness to participate in the methacholine (study I, n = 9), histamine (study II, n = 9), or exercise challenge tests (study III, n = 18). At each session, 80 micrograms ipratropium bromide or placebo were inhaled in a double-blind randomized fashion. After ipratropium bromide, the mean specific airway resistance (SRaw) decreased from 10.4 to 4.9 (study I, p less than 0.01), 9.3 to 5.4 (study II, p less than 0.05), or 7.8 to 5.1 cm H2O.s (study III, p less than 0.01), respectively. Mean methacholine provocation concentrations necessary to increase SRaw by 100% were 0.43 after placebo and 8.60 mg/ml after ipratropium bromide (p less than 0.01), the respective values after histamine challenges were 1.32 mg/ml after placebo and 2.25 mg/ml after ipratropium bromide (p less than 0.01). In the exercise challenges, the individual responses varied largely with a mean maximum percent increase in SRaw of 231% after placebo and 173% after ipratropium bromide pretreatment (p less than 0.05). Therefore, ipratropium bromide offers bronchodilation and protection against a variety of stimuli and should more often be considered as an effective and safe drug for asthma treatment.

Adult↗
PubMed1992

Influence of short-term passive smoking on symptoms, lung mechanics and airway responsiveness in asthmatic subjects and healthy controls.

We studied the acute effect of passive smoking on symptoms, lung mechanics and airway responsiveness. Twenty four patients with mild to moderate bronchial asthma (11 male and 13 female; mean(SD) age 34(15) yrs; forced expiratory volume in one second (FEV1) 91(17) % pred) were investigated. Sixteen of them had a history of passive smoke-induced respiratory symptoms. For comparison we studied 16 controls (7 male and 9 female; mean(SD) age 31(9) yrs; FEV1 106(13) % pred). On two different days, the subjects were exposed in an exposure chamber for one hour to either ambient air (Sham) or environmental tobacco smoke (ETS). During exposure to ETS, the mean concentrations of particles and CO were 3,095 micrograms.m-3 and 20.3 ppm, respectively. Before and immediately after exposure, symptoms and lung mechanics were assessed, followed by an inhalation challenge to determine the provocative concentrations of methacholine necessary to increase specific airway resistance (sRaw) by 100%, (PC100sRaw), and to decrease FEV1 by 20% (PC20FEV1). In the asthmatic subjects, during Sham exposure, mean (SEM) decrease of sRaw and FEV1 was 0.23(0.22) cmH2O.s and 0.04(0.03) l, respectively, (NS). During ETS, mean(SEM) decrease of sRaw and FEV1 was 0.55(0.46) cmH2O.s and 0.13(0.06) l, respectively. The significance of this decrease, however, disappeared when taking into account the individual variability of FEV1. Geometric mean(SEM) PC100sRaw and PC20FEV1 were 0.35(1.32) and 0.23(1.34) mg.ml-1 after Sham, and 0.34(1.37) and 0.28(1.36) mg.ml-1 after ETS, respectively, with no difference between the two study days. In the controls, the two exposure conditions did not exert any significant effects on sRaw, FEV1 and airway responsiveness.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1992

[The effect of flupirtine on respiratory drive in healthy probands and patients with various lung diseases].

We investigated the effect of a novel analgesic compound, flupirtine on the respiratory center in 8 healthy controls and patients with lung emphysema (n = 6), bronchial asthma (n = 7) and lung fibrosis (n = 5). All patients received a in a double blind, randomized fashion on three separate study days 100 mg and 200 mg flupirtine and placebo, respectively. Respiratory drive was estimated from measurements of CO2-rebreathing curves and mouth occlusion pressure at rest and during CO2-rebreathing performed before, 1.5 and 3 hours after medication. We were unable to detect any significant depression of respiratory drive neither in the controls nor in the patients and therefore suggest that flupirtine is a safe analgetic compound even in patients with severe obstructive and restrictive lung function impairment.

Airway Resistance↗
PubMed1992

[Invasive aspergillosis in cavitary lung sarcoidosis].

Pulmonary sarcoidosis is a granulomatous disorder of unknown origin with a favorable outcome in most patients. However in about 5-10% progressive fibrosis is observed and may lead to further complications. We report on a 49 year-old woman with sarcoidosis with fibrotic changes and cavities in both upper lobes, who developed an upper lobe infiltration resistant to antibiotic treatment. Histologic examination of bronchial biopsy specimen revealed invasive aspergillosis. Therapy with Amphotericin B and Flucytosin was followed by marked clinical and radiological improvement.

Aspergillosis↗
PubMed1991

[The effect of oral N-acetylcysteine on glutathione concentration in bronchoalveolar lavage of patients with fibrosing lung diseases].

Glutathione (GSH) is an important constituent in protecting the cellular elements within the lower respiratory tract against oxydants. We measured GSH in bronchoalveolar lavage fluid (BAL) in twelve patients with lung fibrosis and compared the data to eight healthy controls. GSH in BAL was 0.71 +/- 0.34 mumol/l in patients with lung fibrosis and 0.88 +/- 0.35 mumol/l in the controls (p greater than 0.05). After relating GSH on the volume of the epithelial lining fluid (ELF), determined by the urea method, GSH/ELF was 93 +/- 71 mumol/l in lung fibrosis and significantly different (p less than 0.005) from 387 +/- 240 mumol/l in the controls. In seven patients (four lung fibrosis, one desquamative pneumonitis, two asbestosis) GSH in BAL was determined before and after seven days of medication with 1800 mg N-acetylcysteine/day. We observed a significant increase of GSH in BAL from 0.93 +/- 0.46 to 1.56 +/- 0.92 mumol/l. Our observations confirm that in patients with lung fibrosis the protective ability against oxydants is diminished and that one parameter of the antioxydative capacity (GSH) can be increased in BAL by oral administration of N-acetylcysteine. Further studies are necessary to investigate the clinical and therapeutic implications of our findings.

Acetylcysteine↗
PubMed1991

Acute effect of passive smoking on lung function and airway responsiveness in asthmatic children.

The effect of a 1-hour exposure at rest during passive cigarette smoking (20 ppm CO) or Sham was investigated in 11 children with bronchial asthma (age range, 8-13 yr; ten boys, one girl). Nine of the subjects were on regular therapy with inhaled beta 2-agonists and disodium cromoglycate. Both drugs were withheld at least 6 hours prior to each study session. Exposure was performed in an environmental chamber. Before and immediately after exposure, lung function and symptom scores were determined. After exposure, a histamine inhalation challenge was performed to determine the concentrations that caused a 100% increase in SRaw (PC100SRaw) and a 20% fall in FEV1, (PC20FEV1). Mean (SD) SRaw before and after Sham was 8.7 (3.6) and 9.0 (3.2) cmH2O.s, and mean FEV1 (SD) was 1.97 (0.32) and 1.98 (0.40) L, respectively. Before and after cigarette smoking, mean SRaw (SD) was 10.4 (5.3) and 9.4 (3.3) cmH2O.s, and mean FEV1 (SD) was 1.95 (0.37) and 1.94 (0.35 L, respectively. Geometric mean (SD) PC100 SRaw and PC20FEV1 after Sham was 1.39 (3.0) and 0.70 (2.7) mg/mL, and after passive smoking 1.65 (2.5) and 0.96 (2.3) mg/mL, respectively. There were no statistical differences in lung function and PC values between Sham and passive cigarette smoking. The main symptoms during passive smoking were irritation of the eye and the nasopharynx. Our observations suggest that in children with mild bronchial asthma 1 hour of passive cigarette smoking does not cause consistent changes of lung function and bronchial responsiveness.

Adolescent↗
PubMed1991

Comparison of refractoriness after exercise- and hyperventilation-induced asthma.

To study the relationship of bronchoconstriction and refractoriness we performed pairs of exercise and hyperventilation tests in 15 patients (mean [SEM] age 28.5 [2.8] years) with a history of exercise-induced asthma. Mean (SEM) maximum specific airway resistance (SRaw) increased during the first exercise test to 33.9 (4.5) and during the second exercise test to 29.8 (5.2) cmH2O x s (n.s.). Mean (SEM) maximum specific airway resistance (SRaw) increased during the first hyperventilation test to 44.0 (5.9) and during the second hyperventilation test to 27.4 (3.3) cmH2O x s (p less than 0.01). Mean maximum bronchoconstriction after corresponding exercise and hyperventilation tests did not differ statistically. There was a significantly larger inter-individual variability in the airway response to hyperventilation (p less than 0.001). From these data we suggest that similar refractoriness can be observed after both exercise and hyperventilation.

Adolescent↗
PubMed1991

Effect of 0.25 ppm nitrogen dioxide on the airway response to methacholine in asymptomatic asthmatic patients.

In asthmatic patients, short-term exposure to nitrogen dioxide at low concentrations has been reported to result in a nonuniform airway response to various bronchoconstrictive stimuli. We therefore investigated in 11 patients with mild and stable asthma with normal baseline airway tone the effect of 0.25 ppm nitrogen dioxide on the airway response to methacholine. On 2 separate days, the subjects inhaled either 0.25 ppm nitrogen dioxide or filtered air (sham) during 20 min of tidal breathing followed by 10 min of bicycle exercise at room temperature (mean exercise ventilation 30 L/min). Methacholine inhalation tests were performed 1 h after the end of exercise to determine the methacholine concentration necessary to increase SRaw by 100% (PC100SRaw). On a third day, a methacholine challenge was done without previous exposure (control). Mean (SEM) exercise-induced increase of SRaw was 80 (24) % after sham and 82 (25) % after nitrogen dioxide, which was not significantly different (p greater than 0.10). PC100SRaw did not differ on the 3 occasions, geometric mean values (variability of mean) being 0.41 (1.6). 0.41 (1.6), and 0.46 (1.5) mg/ml after sham, nitrogen dioxide, and control, respectively (p less than 0.10). We therefore conclude that in patients with mild and stable asthma short-term exposure to 0.25 ppm nitrogen dioxide during rest and exercise does not increase methacholine responsiveness 1 h after exposure.

Adolescent↗
PubMed1991

Value of CD-1-positive cells in bronchoalveolar lavage fluid for the diagnosis of pulmonary histiocytosis X.

Pulmonary histiocytosis X is characterized by an accumulation of CD-1-positive histiocytosis X cells in the lung, which also can be found in the bronchoalveolar lavage fluid (BALF). However, it has recently been demonstrated that CD-1-positive cells can also be detected in BALF of patients with other interstitial lung diseases and in healthy smokers. We therefore examined the frequency of CD-1-positive cells in a pool of patients with different pulmonary disorders, according to their smoking habits and diagnoses. We have studied the bronchoalveolar lavage in patients with pulmonary histiocytosis X (n = 6), sarcoidosis (n = 88), and in 97 patients with other miscellaneous lung disorders by using the immunoperoxidase method to detect CD-1-positive cells on glass slides. All patients with histologically proven histiocytosis X displayed more than 5% CD-1-positive cells, whereas patients with other pulmonary disorders showed no more than 3.6% CD-1-positive BAL cells. The dividing line of 5% CD-1-positive cells was not influenced by patients' smoking habits. The identification of CD-1-positive cells in BALF appears to be useful in diagnosing pulmonary histiocytosis X.

Antigens, CD↗