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Biomedical subjects

M F Radermecker

Publications and source records attributed to M F Radermecker.

At least 37 records · Page 2Linked to original sources
PubMed1994

Acute bronchial and hematologic effects following inhalation of a single dose of PAF. Comparison between asthmatics and normal subjects.

This study compared the acute bronchial and hematologic effects of inhaled platelet activating factor (PAF) (30 micrograms as a single dose) in 19 patients with mild asthma and 19 normal subjects. Each subject underwent a methacholine bronchial challenge 1 week before PAF challenge to determine the concentration of methacholine causing a 20 percent fall in FEV1 (PC20M). On the day of PAF challenge, specific conductance (SGaw), FEV1, FEF25-75, and platelet and leukocyte counts were measured before, and 5, 10, 15, and 20 min after PAF inhalation. Changes in pulmonary and hematologic parameters were expressed as percent of control (saline solution/ethanol solution). Unlike normal subjects, subjects with asthma had bronchial hyperresponsiveness to methacholine: geometric mean (range): 0.59 mg/ml (0.07 to 9.8) vs > 32 mg/ml. Acute bronchial obstruction over the first 20 min after PAF inhalation was more pronounced in asthmatics than in normal subjects whatever the functional index considered (p < 0.01). In asthmatics (n = 19), mean (SEM) maximal fall in SGaw, FEV1, and FEF25-75 reached 50 percent (6), 11 percent (4), and 19 percent (5), respectively, while in normal subjects (n = 19) the maximal decreases were 24 percent (6), 4 percent (1), and 6 percent (1), respectively. In asthmatics, no correlation was found between log PC20M and log fall in FEV1 after PAF (r = 0.04 p > 0.05). In asthmatics and normal subjects, inhaled PAF caused a transient fall in neutrophils and monocytes by 5 min followed by a full recovery at 15 min and 20 min. These hematologic changes were not significantly different between the two groups. While not correlated with their airway responsiveness to methacholine, asthmatics, compared with normal subjects, develop an exaggerated acute airway obstruction in response to PAF. In contrast, hematologic changes induced by PAF do not differ between asthmatics and normal subjects.

Administration, Inhalation↗
PubMed1993

Plasma histamine and bronchial reactivity in allergic asthma.

Histamine is an important mediator of allergic inflammation and bronchial hyperresponsiveness (BHR), a hallmark of asthma. Studies on the relationship between plasma histamine and BHR in allergic asthmatic patients have yielded controversial results. We therefore measured plasma histamine and bronchial reactivity in 30 nonsmoker volunteers taking no medication. Eleven were normal subjects; 19 were stable, mildly allergic asthmatic patients. Venous blood was taken to measure blood cells and basal plasma histamine by radioimmunoassay. After blood sampling, all subjects underwent a measurement of PC20M (concentration of methacholine causing a 20% fall in FEV1). Mean plasma histamine levels were 0.21 +/- 0.1 ng/ml and 0.44 +/- 0.3 ng/ml in normal and asthmatic subjects, respectively (P < 0.05). We found a significant increase of blood eosinophils and basophils in asthmatic patients, and a positive correlation between plasma histamine and circulating basophils. PC20M was greater than 16 mg in normal volunteers, and mean PC20M was 2.1 +/- 2 mg/ml in asthmatic patients. PC20M did not correlate with plasma histamine levels, but it did so negatively with blood eosinophils. The increased plasma histamine concentration in mildly atopic asthmatic patients might be a consequence of the high basophil releasability of atopics and the higher basophil counts in allergic asthma. Plasma histamine is thus unlikely to be a determinant of BHR in asthma.

Adolescent↗
PubMed1993

Basophil releasability in patients with hymenoptera venom allergy.

Basophils in about 15% of subjects allergic to hymenoptera venom do not release histamine in the presence of antigen. Little is known on the basophil releasability in these patients. We therefore measured maximum percent leukocyte histamine release to antigen (Vespula venom), anti-IgE and formylmethionylphenylalanine (FMP) in 39 patients allergic to wasp venom and compared our results according to basophil responsiveness to antigen. Mean maximum percent histamine release was 39, 34 and 22%, respectively, for venom (100 ng/ml), anti-IgE (0.25 microgram/ml) and FMP (10(-4) M). The amount of histamine specifically released by venom correlated significantly with anti-IgE but not with FMP-induced histamine release. Leukocytes were unresponsive to antigen in 10 subjects. The clinical characteristics and anaphylactic symptoms of these patients were not different from those with antigen-responsive cells. Unresponsive leukocytes responded to FMP in all and to anti-IgE in 8 of the 10 subjects. Mean anti-IgE and FMP-induced histamine release were, respectively, lower and higher than those observed with leukocytes responsive to antigen (p < 0.05). In unresponsive basophils, there was a negative correlation between maximum percent anti-IgE and FMP-induced histamine release. We confirm that basophils of a minority of the subjects allergic to Vespula venom do not release histamine in the presence of antigen. The negative correlation between anti-IgE and FMP-induced histamine release in unresponsive basophils may suggest individual differences in the ratio of Fc epsilon RI and FMP receptors on the surface of basophils.

Adolescent↗
PubMed1992

Histamine-induced inhibition of neutrophil chemotaxis and T-lymphocyte proliferation in man.

Histamine inhibits in vitro human neutrophil chemotaxis and T-lymphocyte proliferation via H2 receptors. The aim of this study was to verify these inhibitory effects of histamine in man in vivo. Healthy volunteers were challenged with histamine by intravenous (1 mg), subcutaneous (1 mg) and inhalatory (2.4 mg) routes. Venous blood was taken before and at different times after challenge. Neutrophil chemotaxis was studied by the Boyden assay and T-lymphocyte proliferation by counting H3-thymidine incorporation in cultured mononuclear cells. Plasma histamine was measured by radioimmunoassay. Histamine infusion caused transient systemic symptoms as well as a significant decrease of neutrophil chemotaxis (mean - 26% +/- 6) and of PHA-pulsed T-lymphocyte proliferation (mean - 16% +/- 6) 4 h after histamine challenge. Subcutaneous injection of histamine caused only a significant decrease of neutrophil chemotaxis (mean - 24% +/- 15) 4 h after injection. Histamine inhalation was well tolerated and caused a significant depression of neutrophil chemotaxis (mean - 40% +/- 15) and of T-lymphocyte proliferation (mean - 27% +/- 6) 2 and 4 h after the challenge. Histamine challenges were always accompanied by a rapid and transient rise in plasma histamine. Inhalation of an H2 agonist (impromidine) but not of an H1 agonist (betahistine) caused a decrease of neutrophil chemotaxis and of T-lymphocyte proliferation. Oral pretreatment with an H2 antagonist (cimetidine) before histamine inhalation prevented histamine-induced decrease of neutrophil chemotaxis and T-lymphocyte proliferation, whereas astemizole, an H1 antagonist, had no effect. In conclusion, during the few hours following administration, exogenous histamine in man causes a depression of neutrophil chemotaxis and T-lymphocyte proliferation via H2 receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1992

Iron content in human alveolar macrophages.

Intracellular iron can be estimated semi-quantitatively by histochemical determination using the ferrocyanide reagent's score. Particle-induced X-ray emission (PIXE) allows accurate determination of various elements including iron in cells and biological fluids. Both techniques have been used to measure iron in alveolar macrophages gathered by bronchoalveolar lavage. The purpose of this study was to investigate the clinical usefulness of the PIXE technique in occupational respiratory medicine and in various pulmonary diseases. Using the PIXE method, we measured the iron content of alveolar macrophages in healthy subjects, with and without occupational exposure to iron dust, and in patients with pulmonary diseases (chronic obstructive pulmonary disease (COPD), lung cancer, Goodpasture's syndrome). Our results were then compared with those obtained with the ferrocyanide reagent. Intramacrophagic iron was 0.33 +/- 0.21 micrograms.10(-6) (mean +/- SD) cells in healthy non-smoking subjects without occupational exposure. Intramacrophagic iron was increased in smokers, iron-steelworkers, and in patients with COPD or lung cancer even in the absence of pulmonary haemorrhage. The two patients with Goodpasture's syndrome had high intramacrophagic iron content. About 80% of the whole bronchoalveolar lavage fluid iron content was in the cells. Mean iron content of blood monocytes, lymphocytes and neutrophils of eight healthy subjects was significantly lower than that of alveolar macrophages. A significant correlation was found between iron determination by the PIXE method and the ferrocyanide reagent's score (r = 0.89). We conclude that intramacrophagic iron may be increased in steelworkers and subjects with pulmonary haemorrhage, but also in asymptomatic smokers, in COPD and lung cancer patients without occupational exposure to iron dust.

Anti-Glomerular Basement Membrane Disease↗
PubMed1991

Cutaneous and basophilic sensitivity to substance P and gastrin in non-atopic versus atopic subjects.

We compared the cutaneous reaction to intradermal injection of substance P, gastrin and histamine in asymptomatic atopic subjects with a history of hay fever and/or asthma versus non-atopic healthy volunteers. We also studied in these two groups the basophilic histamine release induced by substance P and gastrin with that obtained with anti-human IgE and Con A. Intradermal injection of substance P (3-300 pM) and gastrin (3-30 pM) caused a wheal and flare reaction which was comparable in both groups of subjects. Substance P 10(-4)M caused a mean basophilic histamine release of about 15% in atopic and non-atopic subjects. Gastrin was not effective in this model. Anti-IgE and Con A-induced histamine release was significantly higher in atopic than in non-atopic volunteers.

Adult↗
PubMed1991

Effect of histamine on tumor necrosis factor production by human monocytes.

This study was aimed at evaluating the effect of histamine on tumor necrosis factor (TNF alpha) secretion by purified human blood monocytes. TNF alpha was measured by radioimmunoassay. Histamine caused a dose-dependent inhibition of lipopolysaccharide-induced TNF alpha production from human blood monocytes, averaging maximally 50% at 10(-5) M. Preincubation of mononuclear cells with an H2 antagonist (cimetidine), but not with an H1 antagonist (promethazine) prevented this inhibitory effect of histamine. In conclusion, histamine causes, in vitro, a depression of TNF alpha secretion by human monocytes through activation of H2 receptors.

Adult↗
PubMed1990

Substance P-induced histamine release from human basophils, skin and lung fragments: effect of nedocromil sodium and theophylline.

We compared histamine release induced by substance P with those obtained with classical secretagogues on human basophils, lung and skin fragments. We also tested the capacity of nedocromil sodium and theophylline to inhibit histamine release in these 3 experimental models. Substance P (10(-4) M) caused a noncytotoxic histamine release (about 10% of total) from basophils, lung and skin fragments. Substance P-induced histamine release was always smaller than that obtained with optimal doses of anti-IgE, formyl-methionine phenylalanine or compound 48/80. Nedocromil sodium did not prevent secretagogue-induced histamine release from basophils or sliced skin. In contrast, it significantly inhibited anti-IgE- or substance P-induced histamine release from human lung. Theophylline caused a dose-related inhibition on these 3 models. We conclude that substance P is a modest secretagogue for human basophils and mast cells, and that skin and lung mast cells are heterogeneous with respect to their response to nedocromil sodium.

Adult↗
PubMed1990

[Plasma histamine and exercise-induced bronchospasm].

The pathogenesis of bronchospasm of effort is not yet elucidated and it is probable that is determined by multiple factors. In this study we have tested the role of mastocytes in taking as an index of their activation the fluctuation of plasma histamine levels during repeated exercise tests. We will show that asthmatic subjects who develop bronchospasm on effort have a significant rise (times 3) in their level of serum histamine whilst normal subjects don't show much change. Furthermore in a repeated effort test we have observed a strict parallelism between the occurrence of bronchospasm of effort and a rise in plasma histamine levels. These different observations enable us to consider that the activation of mastocytes and the liberation of mediators which follow play an important role in the pathogenesis of bronchospasm of effort.

Adolescent↗
PubMed1989

[Anti-inflammatory effects of histamine].

Most of the body's histamine is stored in the granules of tissue mast cells and blood basophils. Free histamine regulates gastric acid secretion, acts as a neurotransmitter in the central nervous system and is a potent mediator of allergic inflammation. Histamine may also exert negative influences on human inflammatory cells in vitro. Evidence is provided here that the administration of histamine in man may depress the chemotactic response of the PMNs and spontaneous or pulsed T-lymphocyte proliferation. Thus, histamine has indeed, in man, some antiinflammatory actions which may explain the increased sensitivity of asthmatics to respiratory infections.

Anti-Inflammatory Agents, Non-Steroidal↗