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Biomedical subjects

P Camner

Publications and source records attributed to P Camner.

At least 73 records · Page 4Linked to original sources
PubMed1989

Individual differences in regional deposition of 6-micron particles in humans with induced bronchoconstriction.

The effect of induced bronchoconstriction on regional lung deposition of 6 microns aerodynamic diameter 99mTc-labeled Teflon particles was studied in eight healthy non-smokers. The Teflon particles were inhaled at 0.5 l/s from a 25-l glass bulb with 8-12 maximally deep breaths on four consecutive days. For three exposures, various degrees of bronchoconstriction were induced using an aerosol of methacholine bromide before the inhalation of the Teflon particles. For the fourth (control) exposure, bronchoconstriction was induced after the inhalation of the Teflon particles. The degree of bronchoconstriction was quantified by measurements of airway resistance (Raw) using a whole-body plethysmograph. The fraction of alveolarly deposited particles in the lung (FAD) was estimated by measurements of radioactivity in the lung immediately after inhalation of the Teflon particles and 6 h later. Earlier studies have shown that when the mucociliary transport is stimulated with the cholinergic aerosol used in this study, the 6-h retention values (Ret6) are similar to the 24-h values. Within the subjects there was a close relationship between Raw and Ret6 with a decrease of Ret6 with increased Raw. This decrease varied markedly among the subjects. The relationship between Raw and Ret6 calculated from the model by the Task Group on Lung Dynamics, in which the airway diameters were varied, agreed with our experimental data. On an average, airway resistance of 1 and 2 cm H2O.s/l correspond to FAD of about 50% and 25%, respectively.

Administration, Inhalation↗
PubMed1989

Estimation of pH in individual alveolar macrophage phagolysosomes.

A method for measurement of phagolysosomal pH in individual alveolar macrophages based on a cytofluorometric technique with fluorescein-labeled silica particles (FSP) as a probe was developed. The size of the FSP, 3.0 or 5.0 microns, did not affect the result of the pH measurements. The average pH values, range 5.1-5.5, of individual particles in macrophages from three rabbits agreed well with the pH values obtained in a macrophage population using a fluorescence spectrometer and the FSP. The variation of pH in phagolysosomes in alveolar macrophages from five rabbits was investigated. Measurements were performed 3, 6, and 24 h after addition of the FSP in cells containing one particle as well as in cells containing two particles. The variation in pH was small, with a coefficient of variation less than 10% in all rabbits at all times. There was a significant correlation between values obtained from two phagolysosomes in the same cell, indicating a cell factor responsible for 10-30% of the total variance. The fact that the variation of pH is small in normal, untreated rabbit alveolar macrophages should be of importance when estimating alveolar clearance of inorganic particles due to dissolution in the acid phagolysosomal milieu.

Animals↗
PubMed1989

Human lung deposition of particles suspended in air or in helium/oxygen mixture.

Deposition in mouth and throat and the fraction of alveolarly deposited particles in the lung of 3.6- to 3.8-microns Teflon particles labeled with 99mTc were estimated in nine healthy subjects. The particles were inhaled in air or helium/oxygen mixture with a flow of 0.5 l/s by subjects with or without induced bronchoconstriction. The bronchoconstriction (two- to threefold increase in airway resistance) was induced by an aerosol of methacholine bromide. As the Reynolds number is three times lower for the helium/oxygen mixture than for air, and the sedimentation rate of the particles is about the same in both, a different regional deposition between particles suspended in air and helium/oxygen mixture should be due to turbulence. Deposition in mouth and throat did not differ significantly between air and the helium/oxygen mixture. The alveolarly deposited fraction tended to be larger for unconstricted airways and was significantly larger for constricted airways for inhalations in the helium/oxygen mixture compared to air. In real life, air pollutants and therapeutic aerosols may be inhaled with larger flow rates and broncho-constriction may be more pronounced in patients, so that deposition of particles due to turbulence can be important.

Administration, Inhalation↗
PubMed1988

Rabbit lung after inhalation of lithium chloride.

Rabbits were exposed to aerosols of lithium chloride in metal concentrations of 0.6 and 1.9 mg/m3 (mass median aerodynamic diameter of 1 micron) for 4-8 weeks, 5 days/week, 6 h/day. The lungs were studied by light and electron microscopy, with particular reference to inflammatory changes, structure of alveolar macrophages and alveolar epithelial cells. Macrophages recovered by lung lavage were studied by light and electron microscopy and their oxidative metabolic activity was measured. The content of phospholipids was analysed in lung tissue. Exposure to lithium produced no significant effects. It thus seems that Li+ is less toxic to the lung than the other metals investigated with the same test system, e.g. Ni2+, Cd2+, Co2+, Cr3+ and Cr6+.

Administration, Inhalation↗
PubMed1988

Alveolar macrophages in rabbits after combined exposure to nickel and trivalent chromium.

Rabbits were exposed to a combination of 0.7 mg/m3 Ni2+ as NiCl2 and 1.2 mg/m3 of Cr3+ as Cr(NO3)3, to 0.6 mg/m3 of Ni2+ as NiCl2, or to filtered air for about 4 months, 5 days/week and 6 hr/day. Alveolar macrophages were recovered by lung lavage and studied by light and electron microscopy. Metabolic activity, phagocytic capacity and lysozyme activity in the macrophages were studied. After the combined exposure, the effects on lung weight, number of macrophages, and appearance of surface and number of intracellular laminated inclusions in these cells were more than additive. These effects might be explained by a combination of increased production by Ni2+ and impaired catabolism of surfactant by Cr3+. Because the metal concentrations used were not far above occupational threshold limit values, combined exposures to nickel and trivalent chromium should be considered more seriously.

Animals↗
PubMed1988

Intraphagosomal pH in alveolar macrophages after phagocytosis in vivo and in vitro of fluorescein-labeled yeast particles.

The pH in phagolysosomes of rabbit alveolar macrophages was studied using yeast particles labeled with fluorescein isothiocyanate (FITC). The yeast particles were added to the macrophages in vitro a few hours or 1 day after they had been lavaged from the lung and in vivo 3 h or 1 day before the lungs were lavaged. Intracellular pH was estimated from the ratio between the fluorescence intensity at wavelength 519 nm with excitation at wavelengths of 495 and 450 nm. In both the in vitro and in vivo experiments pH decreased significantly during the first hours after lavage, but after a few hours reached almost the day-2 levels, i.e., 4.9-5.4. The decrease in pH was related to time after lavage and not to time after phagocytosis of the particles. It is suggested that intracellular measurements of pH in alveolar macrophages should be combined with determinations of lung clearance of metal particles.

Animals↗
PubMed1987

Morphology and release of lysozyme following exposure of rabbit lung macrophages to nickel or cadmium in vitro.

Lung macrophages lavaged from 7 rabbits were incubated with 0, 3, 6, 12 and 24 micrograms/ml of nickel as NiCl2 and macrophages from 4 rabbits were incubated with 0, 0.1, 1, 3 and 6 micrograms/ml of cadmium as CdCl2. After 2 days lysozyme activity in the medium in which the macrophages were cultivated, was estimated using a technique with agar plates prepared with heat-killed Micrococcus lysodeikticus. Macrophage morphology was examined by scanning and transmission electron microscopy. For nickel there was a dose-related inverse relationship between the lysozyme activity and concentration of nickel. Many macrophages exposed to the higher nickel concentrations had a rounded form and, thus, the surface area of each cell which came in contact with the glass appeared to be less than that for control macrophages. There was, however, no increase in the number of macrophages detached from their glass support. Cadmium exposure did not influence lysozyme levels of activity, in spite of morphological indications of cell toxicity. From the present study we conclude that the decreased lysozyme activity seen previously in vivo after nickel inhalation is likely to be due to a direct effect of nickel ions on macrophages and that the increased lysozyme activity seen in vivo after cadmium inhalation is probably a secondary effect, subsequent to inflammation.

Animals↗
PubMed1987

Dissolution of two arsenic compounds by rabbit alveolar macrophages in vitro.

The ability of rabbit alveolar macrophages to dissolve two arsenic compounds, 74As-labeled lead arsenate and arsenic trisulfide, was studied in vitro. The solubilities in water of these two compounds are related differently to pH. The solubility of lead arsenate increases and that of arsenic trisulfide decreases with decreasing pH. The radiolabeled particles were incubated with and without macrophages for up to 3 days, whereafter the amount of 74As in soluble form and the amount in particle form and/or bound to macrophages were determined. The results strongly support the hypothesis that the dissolution of particles by macrophages is influenced by the acid milieu in the phagosomes. About 14% of the 74As-labeled lead arsenate particles incubated for 3 days with the macrophages was released into the culture medium, compared with about 2% of the particles incubated with the culture medium without macrophages. With the arsenic trisulfide particles, less soluble 74As was released into the medium in samples with macrophages than in samples without macrophages, although the solubility in all incubations was considerably greater than that for lead arsenate. The results indicate that dissolution in the phagosomes of the macrophages may be of great importance for the clearance of particles such as lead arsenate, which are more soluble at pH 4 than at pH 7.

Animals↗
PubMed1987

Fibronectin concentrations in lung lavage fluid after inhalation exposure to low levels of metals.

Groups of rabbits were exposed by inhalation to chlorides of cobalt, nickel, and manganese as well as to tri- and hexavalent chromium at metal concentrations ranging from 0.4 to 3.9 mg/m3 for 1-4 months (5 days/week, 6 hr/day). Fibronectin content and lysozyme (muramidase) activity in lavage fluid were measured after all treatments and in alveolar macrophages after treatment with nickel chloride. In the lavage fluid no marked changes were seen in fibronectin content and lysozyme activity after exposure to tri- or hexavalent chromium or manganese. Nickel exposure significantly decreased the lysozyme activity in the lavage fluid and in the macrophages whereas the fibronectin content was unchanged in the lavage fluid and significantly increased in the macrophages. Both fibronectin content and lysozyme activity were increased markedly in the lavage fluid after cobalt exposure.

Administration, Inhalation↗
PubMed1987

Nodular accumulation of type II cells and inflammatory lesions caused by inhalation of low cobalt concentrations.

Eight rabbits were exposed to 2 mg/m3 and eight to 0.4 mg/m3 of cobalt as CoCl2 for 14-16 weeks (5 days/week, 6 hr/day). Eight rabbits were used as controls. Light microscopic examination of the lungs showed nodular accumulation of alveolar type II cells in all cobalt-exposed rabbits. Abnormal macrophage reaction was observed in all eight rabbits exposed to the high dose and in five of the eight exposed to the low dose. Interstitial inflammation was present in all the rabbits exposed to the high dose and in half of the rabbits exposed to the low dose. Ultrastructural morphometric examination revealed no significant increase in the volume density of type II cells in the cobalt-exposed animals, as the nodular accumulation of these cells was balanced by an increased number of interjacent fields devoid of type II cells. In cobalt-exposed lungs, there was focal swelling of both type I and type II cells, and some of the latter lacked microvilli. The effect pattern after CoCl2 exposure was thus clearly different from those patterns seen after exposure to other toxic metals. We speculate that nodular accumulation of type II cells represents the primary lesion in CoCl2-exposed lungs and that the proliferation of such cells in interjacent areas might be suppressed by a feedback mechanism regulating surfactant production in the terminal airspaces.

Animals↗
PubMed1987

Alveolar macrophage abnormalities in rabbits exposed to low concentrations of trivalent chromium.

Rabbits were exposed by inhalation to a trivalent chromium compound (Cr(NO3)3) at a mean chromium concentration of 0.6 or 2.3 mg/m3 for about 4 months, 5 days/week and 6 hr/day. Light microscopic examination of the lungs revealed that both chromium levels induced a nodular intraalveolar accumulation of enlarged macrophages with granular, eosinophilic cytoplasm. Some macrophages were multinucleated and some showed advanced degenerative changes with disruption of cellular borders and nuclear pyknosis. The changes were most prominent in rabbits exposed to the high concentration and were in some areas associated with a mild interstitial infiltration of lymphocytes, neutrophils, and eosinophils. Electron microscopic examination of macrophages lavaged from the lungs revealed numerous enlarged lysosomes with membranous structures, distinct rounded inclusions, which by X-ray microanalysis were found to contain high amounts of chromium, and increased numbers of laminated inclusions probably representing ingested surfactant. The number of macrophages with a smooth surface was significantly increased. The macrophages in the lung tissue showed the same changes and in addition nodules of multinucleated "giant" cells were found. Morphometric estimation of the volume density of the type II cells did not reveal any significant differences between controls and rabbits exposed to the high concentration of chromium. In spite of the elevated number of laminated structures in the macrophages the amounts of phosphatidylcholine and 1,2-dipalmitoylphosphatidylcholine were not significantly increased in the lung. This indicates a reduced catabolism of surfactant by the alveolar macrophages.

Animals↗
PubMed1987

Lysozyme activity in ultrastructurally defined fractions of alveolar macrophages after inhalation exposure to nickel.

Rabbits were exposed to 0.6 mg/m3 of nickel as NiCl2 for about one month. After exposure, alveolar macrophages were lavaged from the lung and divided into three fractions by elutriation. Laminated structures in the macrophages were related to fraction number so that the fractions with the largest cells contained the highest number of structures. The lysozyme activity decreased in unfractionated as well as in fractionated macrophages from nickel exposed rabbits. The decrease was most pronounced in the fraction with the smallest macrophages and smallest number of laminated structures. Therefore the pronounced decrease in lysozyme activity seen in this and earlier studies is not caused by the increased amount of surfactant material. Increased amount of surfactant is a hallmark of nickel inhalation exposure and the surfactant material is responsible for the morphological and metabolic effects of the macrophages. The decreased lysozyme activity is probably a direct effect of nickel on the macrophages.

Animals↗
PubMed1987

Regional deposition in human lung of 2.5 microM particles.

Regional deposition in the lung of 111In-labelled Teflon particles with an aerodynamic diameter of 2.5 micron was studied in eight healthy nonsmokers. The particles were inhaled at 0.5 l/sec with maximally deep breaths. Bronchoconstriction was induced by inhalation of a methacholine bromide aerosol, for one exposure series before (provocation experiment) and for one exposure series after (control experiment) inhalation of the Teflon particles. Airway resistance (Raw) was measured with a whole-body plethysmograph before and after the induction of bronchoconstriction and increased on an average by a factor of 3-4. The total lung deposition, in percent of the inhaled radioactivity, was 83 +/- 6% (mean +/- SD) for the control experiment and 84 +/- 5% for the provocation experiment. Alveolar deposition, estimated as the percentage retention of lung deposition after 24 hrs (Ret24), was significantly lower in the provocation experiment than in the control experiment, 42 +/- 10% and 77 +/- 12%, respectively. Ret24 varied greatly among the subjects in the control experiment; for example, individual tracheobronchial deposition varied by a factor of 5. Ret24 was not related to FEV1, FVC or Raw. The Ret24 values in the two exposure series correlated significantly indicating an individual factor. Retention at 3 and 24 hrs correlated strongly, r = 0.94. This implies that radionuclides with half-lives of a few hours, e.g., 99mTc, can be used in studies of regional lung deposition when mucociliary transport system has been stimulated.

Adult↗
PubMed1987

Deposition of large particles in human lung.

Twenty-four nonsmoking males, all without history of pulmonary disease, were randomly divided into four groups of six subjects each. The subjects in each group inhaled monodisperse Teflon particles labelled with 111In (half-life 2.83 days); 8.2, 11.5, 13.7 and 16.4 micron aerodynamic diameter, respectively. Radioactivity in head and throat, lung and stomach was determined after 0, 3 and 24 hrs using a profile scanner. For some subjects radioactivity was also determined using a whole-body scanner at 3.5 and 24 hrs. After the 24-hr determination the subjects inhaled labelled Teflon particles again, this time with a filter in front of the mouth. Average values for total deposition in the body, obtained using a profile scanner, whole-body scanner and filter measurements, agreed fairly well. Lung retention values obtained by whole-body and profile scanning also agreed well. The average deposition in the lung, expressed as a percentage of total deposition, was 49, 31, 21 and 13% for the four particle sizes (8.2-16.4 micron). Alveolar deposition, determined as retention at 24 hrs and expressed in percent of total deposition, was 15, 4, 4 and 1%. For the smallest particle sizes the deposition values agreed with earlier investigations. However, for the larger particles the two deposition values were higher than expected when compared to earlier studies.

Administration, Inhalation↗
PubMed1987

Influence of ambroxol on tracheobronchial clearance in simple chronic bronchitis.

The influence on tracheobronchial clearance of ambroxol, a metabolite of bromhexine, was investigated by measuring the lung retention of inhaled 6 micron monodisperse Teflon particles labelled with 99mTc. Fourteen subjects with simple chronic bronchitis, who belonged to a "responder" group in an earlier study on the subjective effects of ambroxol, were examined using a double-blind cross-over design comparing 120 mg ambroxol daily and placebo. On commencing the study and after each 2-week treatment period, the subjects were examined for mucociliary clearance and clearance by voluntary coughing. Treatment did not influence mucociliary clearance or clearance by cough. There is still a possibility that phlegm loosening by cough is enhanced in situations with more hypersecretion.

Adult↗
PubMed1986

Rabbit alveolar macrophages after inhalation of hexa- and trivalent chromium.

Rabbits inhaled aerosols of hexavalent chromium (Na2CrO4) and trivalent chromium (Cr(NO3)3) at concentrations of 0.9 and 0.6 mg/m3 of the metal, respectively, for 4-6 weeks (5 days/week and 6 hr/day). Significantly more macrophages were obtained from the lungs of rabbits exposed to Cr(VI) but not from rabbits exposed to Cr(III) as compared with the controls. Macrophages from rabbits exposed to Cr(III) showed several conspicuous changes. About one-third of the macrophages contained round dark inclusions, 0.5-1.5 micron diameter, rich in chromium. Most cells had very large lysosomes which contained membranous fragments of different sizes surrounded by a more homogeneous matrix. Laminated inclusions similar to the lamellar bodies in the type II cells increased in number as did the percentage of cells with a smooth cell surface. Also macrophages from rabbits exposed to Cr(VI) showed morphological changes. The most pronounced one was enlarged lysosomes which contained short lamellae and electron-dense patchy inclusions. Only Cr(III) produced functional changes of the macrophages. The metabolic activity measured by reduction of nitroblue tetrazolium was increased and the phagocytic activity reduced.

Animals↗
PubMed1986

Rabbit alveolar macrophages after long-term inhalation of soluble cobalt.

Rabbits were exposed to 2 or 0.4 mg/m3 of cobalt as CoCl2 for 14-16 weeks (5 days/week and 6 hr/day). More macrophages were lavaged from the lungs of rabbits exposed to the higher Co2+ concentration, and the diameter and variation of the diameter of the macrophages were significantly larger than in controls. The activity of lysozyme in the lavage fluid and in the macrophages was increased in the two exposed groups. Some macrophages in the exposed animals were large and engorged with intracellular lamellar inclusions and lipid droplets. Most of these cells had a smooth surface. The oxidative metabolic activity measured by reduction of nitroblue tetrazolium was increased in the exposed groups. The number of yeast cell particles attached to the surface of the macrophages was increased in the group exposed to the high concentration, but the number of ingested particles was not affected by cobalt exposure. Apart from the fact cobalt increased lysozyme activity whereas nickel decreased it, cobalt produced the same type of effects on macrophages as nickel did in earlier studies. Cobalt affected only a minor proportion whereas nickel affected most macrophages. This can be explained by the fact nickel produced a general increase in the volume density of the type II cells while cobalt affected the type II cells only in some areas of the lungs.

Administration, Inhalation↗