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Biomedical subjects

T Bury

Publications and source records attributed to T Bury.

At least 73 records · Page 4Linked to original sources
PubMed1992

LY 186655, a phosphodiesterase inhibitor, inhibits histamine release from human basophils, lung and skin fragments.

LY 186655 (Tibenelast, Lilly) is a new phosphodiesterase inhibitor, not derived from the xanthine, possessing bronchodilating activity in animals. The aim of this work was to study the effect of LY 186655 and theophylline on histamine release from human leukocytes, skin and lung fragments. Histamine was measured using a spectrofluorometric method. Both drugs (3 x 10(-5)-3 x 10(-3) M) exhibited a dose-dependent inhibition on anti-IgE (1/2000)-induced histamine release from human leukocytes. At 3 x 10(-3) M, theophylline was significantly more effective than LY 186655 (mean inhibition 94 and 42%, respectively). On lung fragments, theophylline and LY 186655 (3 x 10(-5)-3 x 10(-3) M) caused strong and comparable inhibitory effects on anti-IgE (1/500)-induced histamine release with a mean inhibition reaching maximally 65%. Histamine release induced by compound 48/80 (1 mg/ml) on sliced human foreskin was reduced with both drugs (3 x 10(-3) M) by about 37%. We conclude that LY 186655 inhibits in vitro immunological histamine release from human lung and cutaneous mast cells as well as basophils with a similar pattern of activity to theophylline.

Adult↗
PubMed1992

Role of histamine in the chemotactic deactivation of polymorphonuclear leukocytes following incubation with formylmethionyl peptides.

To clarify the mechanism of chemotactic deactivation of polymorphonuclear neutrophils (PMN) following incubation with the synthetic dipeptide N-formylmethionyl phenylalanine (FMP), we tested the hypothesis that histamine, which is released from leukocytes during incubation with FMP, could explain this inhibition. Human PMN were incubated in the presence or absence of FMP (10(-7) to 10(-5) M) and histamine measured fluorometrically in the supernatant. Washed PMN were then tested in Boyden chambers against FMP (10(-5) M) and other chemoattractants. Incubation of leukocytes with FMP caused a nonpreferential PMN deactivation which was proportionally and kinetically related to FMP-induced histamine release. No histamine release or chemotactic deactivation was observed in the absence of Ca2+ and Mg2+. The inhibitory effect of the peptide was significantly prevented by an H2 blocker or when using basophil-depleted PMN suspensions. Histaminase abolished the capacity of FMP-incubated leukocyte supernatants to decrease PMN chemotaxis. Preincubation of leukocytes with anti-IgE or a sensitizing allergen caused a significant PMN chemotactic deactivation. These results show that histamine which is released during leukocyte incubation with FMP, contributes, at least in part, to the chemotactic deactivation of PMN.

Amine Oxidase (Copper-Containing)↗
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

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↗
PubMed1991

Two years treatment with almitrine bismesylate in patients with hypoxic chronic obstructive airways disease.

Eighty nine patients with hypoxic chronic obstructive airways disease (COAD) were enrolled into the 1 year Vectarion International Multicentre Study-VIMS in 4 centres, Sheffield (UK), and Antwerp, Liege and Namur (Belgium). At the end of the year the remainder were invited to continue taking placebo or almitrine bismesylate (100-200 mg daily) in the same double blind manner for a further 12 months. In the almitrine treated patients mean arterial oxygen tension (Pao2) at the end of the treatment period improved from 7.5 (0.5) kPa to 8.2 (1.3) kPa (p less than 0.01) and arterial carbon dioxide tension (Paco2) fell from 6.1 (0.8) kPa to 5.8 (0.9) kPa (p less than 0.01). Forced expiratory volume in one second (FEV1), forced vital capacity (FVC) and measurements of breathlessness were unchanged. In the placebo treated group changes in the above variables were not significant. Twenty nine patients withdrew from the almitrine group with seven deaths and six cases of peripheral neuropathy, and 22 patients withdrew from the placebo group with six deaths and two cases of peripheral neuropathy. Death rates between the groups were not significantly different. In conclusion, 2 yrs of almitrine treatment (100-200 mg daily) leads to a persistent slight improvement in PaO2 and PaCO2 but no benefit in survival was demonstrated. Patients in this study had a high incidence of drug related side-effects. Lower dose schedules should be investigated.

Almitrine↗
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

Effect of histamine on chemotaxis and phagocytosis of human alveolar macrophages and blood monocytes.

We studied in vitro the effect of histamine on the chemotactic and phagocytic abilities of human blood monocytes and alveolar macrophages. The chemotactic response to activated autologous serum, leukotriene B4 or N-formyl-methionine-L-phenylalanine was similar for macrophages and monocytes. Incubation of monocytes with histamine in picomolar concentrations caused a significant chemotactic inhibition (about 25%). This effect was antagonized by cimetidine but not by promethazine. Histamine did not have an effect on alveolar macrophages chemotaxis or phagocytosis. Thus, histamine, in minute concentrations, exerts, in vitro, a partial inhibitory effect on monocyte chemotaxis through activation of H2-type receptors.

Chemotaxis, Leukocyte↗
PubMed1989

Dose-response and pharmacokinetic study with almitrine bismesylate after single oral administrations in COPD patients.

To better define the dose-effect relationship and the pharmacokinetics of almitrine, sixteen stable hypoxaemic COPD patients received random single oral administrations of almitrine bismesylate 50, 100 and 150 mg or placebo at two-week intervals in a double-blind manner. Resting ventilation, arterial blood gases and plasma almitrine levels were measured. No significant changes were seen after placebo administration. Almitrine 50 and 100 mg caused a significant dose-related improvement in arterial oxygen tension (PaO2) in thirteen of the sixteen patients. Almitrine 150 mg caused little if any additional PaO2 increment. PaO2 returned to near basal values after 24 h. Two patients responded to almitrine 100 and 150 mg only, whereas one patient did not respond at all. Mean PaO2 increases in the sixteen patients were 0.9 kPa (7 mmHg), 1.5 kPa (11 mmHg) and 1.6 kPa (12 mmHg) 3 h after 50, 100 and 150 mg, respectively. A significant mean 0.9 kPa (7 mmHg) decrease in arterial carbon dioxide tension (PaCO2) and a l.min-1 increase in ventilation were observed after almitrine 150 mg. Mean maximum almitrine plasma concentration and area under the curve correlated linearly with dose. The relationship between mean PaO2 improvement and mean almitrine plasma level was curvilinear with a flattening of the curve over plasma levels of 150 ng.ml-1. Almitrine plasma half-life was found to be 116-140 h.

Aged↗
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↗
PubMed1989

[Alveolar proteinosis: restoration of the function of the alveolar macrophages after therapeutic lavage].

The aim of this study was to specify the effect of therapeutic pulmonary lavage on the function of alveolar macrophages in a patient suffering from alveolar proteinosis; we have studied phagocytosis and chemotaxis in cells before and at different times after the lavage. Our results indicate a restoration of the functional properties of the alveolar macrophages in parallel with an improvement in pulmonary function and blood gases under the effects of treatment. These data are in favour with an inhibitory effect of the lipoprotein material on the function of alveolar macrophages and suggest that the deposit of this material is a determining factor in the alteration in the defense mechanisms of the lung.

Adult↗