Search PubMed⌕ Search

Biomedical subjects

P Camner

Publications and source records attributed to P Camner.

At least 91 records · Page 5Linked to original sources
PubMed1986

Rabbit lung after inhalation of hexa- and trivalent chromium.

Rabbits were exposed to aerosols of hexavalent (Na2CrO4) and trivalent chromium (Cr(NO3)3) at concentrations of 0.9 and 0.6 mg/m3 of chromium respectively for 4-6 weeks (5 days/week and 6 hr/day). Three of eight rabbits exposed to Cr(VI) and three of eight rabbits exposed to Cr(III) showed nodular accumulations of alveolar macrophages, similar to the lesions observed in previous experiments after exposure to Ni2+, Cd2+, or metallic nickel. Macrophages from rabbits exposed to Cr(III) usually contained round dark inclusions, large lysosomes, and laminated inclusions similar to the lamellar bodies in the type II cells, and most macrophages from rabbits exposed to Cr(VI) showed enlarged lysosomes. However, the total amount of phospholipids and the volume density of type II cells did not differ significantly between exposed rabbits and controls. Our findings indicate that the macrophages are directly affected by chromium. The accumulation of laminated structures in the alveolar macrophages after Cr(III) exposure might be due to an impaired catabolism of surfactant.

Administration, Inhalation↗
PubMed1986

Spirometric data and penetration of particles to the alveoli.

The percentage retention at 24 hours of 4 micron Teflon particles, aerodynamic diameter about 6 micron, was studied in 29 healthy male volunteers. The particles were inhaled at 0.5l/s with maximally deep breaths. The 24 hour retention correlated significantly with FEV1 and FVC and persisted when the subjects were divided into different categories according to profession and smoking habits. The results suggest that for exposure to metal particles at a size where impaction is an important deposition mechanism--that is, particles larger than a few microns--workers with large FEV1 values may run a greater risk of receiving systemic toxic effects than those with small FEV1 values.

Adult↗
PubMed1986

Regional deposition of particles in human lung after induced bronchoconstriction.

The percentage 24-hr lung retention (Ret24), a measure of penetration to the aveoli, of 4 micron monodispersed Teflon particles, aerodynamic diameter 6 micron, was studied in 8 healthy nonsmokers. The particles were inhaled at 0.2 1/sec with maximally deep breaths. Bronchoconstriction was induced by inhalation of a methacholinebromide aerosol for one exposure before and for one exposure after inhalation of the Teflon particles. Airway resistance (Raw) was measured using a whole body pletysmograph before and after the induction of bronchoconstriction and increased on an average by a factor 2-3. Ret24 was significantly lower when the Teflon particles were inhaled during bronchoconstriction than when bronchoconstriction was induced after inhalation of the Teflon particles, 26 +/- 12% and 48 +/- 6% (mean +/- SD), respectively. These experimental data agree fairly well with data on deposition due to impaction and sedimentation using a lung model where the diameters of the airways were varied so that an increase in airway resistance occurs similar to that produced in our experimental subjects. However, the experimental data tended to be lower than the theoretical ones when the particles were inhaled during the induced bronchoconstriction. In this study, where the mucociliary transport system was stimulated by methacholinebromide, the percentage 3-hr retention (Ret3) was highly correlated with Ret24, r = 0.97, i.e., Ret3 can be used instead of the Ret24. This implies that radionuclides with shorter half-lives which give lower radiation doses, can be used, and that subjects can be studied within shorter periods of time.

Adult↗
PubMed1986

Mucociliary clearance in relation to clinical features in patients with bronchiectasis.

Patients with bronchiectasis collected from a register covering all hospital stays within the county of Stockholm were asked to participate in a study of lung mucociliary clearance. Twenty-one patients inhaled 6 um Teflon particles labelled with 99mTc and radioactivity was measured externally. The patients were also clinically classified. Clearance varied from normal to extremely slow. The average retention at 2 hours was significantly higher in the patients, 65+27%, (mean +/- SD) than in healthy nonsmokers, 36+22%. Clearance was more impaired the more generalized the airway symptoms were, the more continuous they were, and the earlier in life they had started, all features which indicate a coherence with the immotile cilia syndrome, an obvious "model disease" in this context. Clearance was studied separately in two lungs in 18 patients and was similar in both lungs with one exception. A full presentation of this investigation is submitted to Eur. J. Respir. Dis.

Adult↗
PubMed1986

Mucociliary clearance in relation to clinical features in patients with bronchiectasis.

Patients with bronchiectasis were collected from a register covering all hospital stays within the county of Stockholm. They were asked to come for an interview, a clinical examination and to participate in a study of lung mucociliary clearance. The subjects inhaled 6 microns Teflon particles labelled with 99mTc and radioactivity was measured externally. Clearance varied from normal to extremely slow. The average retention of the Teflon particles at 2 h was significantly higher in the 21 patients, 65 +/- 27% (mean +/- SD), than in healthy nonsmokers, 36 +/- 22%. Clearance was more impaired the more generalized the airway symptoms were, the more continuous they were, and the earlier in life they had started; all features which indicate a coherence with the immotile cilia syndrome, an obvious "model disease" in this context. Clearance was studied separately in the two lungs in 18 patients and was similar in both lungs, with one exception.

Adult↗
PubMed1986

Adverse effects of metals on the alveolar part of the lung.

Rabbits were exposed to low levels of metal dust or metal ions by inhalation for 1-8 months, 5 days/week and 6 h/day. Following exposure lung tissue was examined by light and electron microscopy, the lung content of phospholipid was analyzed and the morphology and function of alveolar macrophages were investigated. Metallic nickel dust as well as soluble nickel chloride produced accumulation of macrophages and laminated structures in alveoli and increased volume density of alveolar type II cells. The amount of phospholipids was elevated, mainly due to an increase in disaturated phosphatidylcholine. After one month exposure to metallic nickel dust or soluble nickel chloride, the alveolar macrophages contained surfactant inclusions and were functionally activated. After 3 and 6 months exposure to metallic nickel the macrophages were 'overfed' and inactive. A similar reaction is seen in the human disease pulmonary alveolar proteinosis. Exposure to cadmium chloride gave a similar reaction pattern as nickel did but in addition interstitial alveolitis. One month exposure to cobalt chloride affected the growth pattern of type II cells which formed nodules projecting into the alveolar lumen. Four months exposure to cobalt chloride resulted in further developed type II cell nodules, areas of hyperreactive type II cells, and interstitial inflammation. Copper chloride produced no effects apart from a slight increase in volume density of type II cells. Hexa- and trivalent chromium mainly affected the alveolar macrophages which showed enlarged lysosomes. Thus, different metal ions, in similar concentrations produced different pathological effects in the lung.

Animals↗
PubMed1985

Rabbit lung after inhalation of manganese chloride: a comparison with the effects of chlorides of nickel, cadmium, cobalt, and copper.

Rabbits were exposed to aerosols of MnCl2 (mass median aerodynamic diameter 1 micron) in metal concentrations of 1.1 and 3.9 mg/m3 for 4-6 weeks, 5 days/week, 6 h/day. The effects of alveolar type II cells, phospholipids, alveolar macrophages, and lung structure in general were compared with earlier reported effects of Ni2+, Cd2+, Cu2+, and Co2+. Except for a significant increase in the diameter of the alveolar macrophages after exposure to the higher Mn2+ concentration, no abnormalities were seen. The results of this and earlier studies indicate that these five metal ions have different, specific effects on the alveolar part of the lung.

Animals↗
PubMed1985

Dissolution of metals by human and rabbit alveolar macrophages.

The ability of human and rabbit alveolar macrophages to dissolve 0.1-0.5 micron MnO2 particles in vitro was compared. The amount of Mn added and dissolved from the particles over periods of nought, one, and three days was determined by flame atomic absorption spectrophotometry. The amount dissolved by human and rabbit macrophages was similar; on average 43.1% and 43.9%, respectively, were dissolved within three days. But rabbit and human macrophages dissolved significantly more Mn than was dissolved in the respective culture medium without macrophages after one and three days. It is suggested that the dissolution of particles by alveolar macrophages should be one basic component in any model of alveolar clearance of inorganic particles.

Adult↗
PubMed1985

Long-term lung clearance in humans studied with Teflon particles labeled with chromium-51.

Six healthy nonsmoking males inhaled 4-micron diameter Teflon particles labeled with chromium-51. Lung retention was measured for approximately 300 days. Three subjects inhaled "high-leaching" particles and three "low-leaching" particles. The high-leaching leaching particles leached 0.26%/day in water at 37 degrees C for the first 100 days and the low-leaching particles 0.065%/day. On an average, urine sampled for 24 h contained 0.13% of the lung burden for the high-leaching particles and 0.02% for the low-leaching particles. Thirty percent of the long-term clearance occurred with a fast phase, with half-times ranging from 4.5-45 days, and 70% with a slow phase, with half-times ranging from 200-2500 days. The fast phase was similar for the high-leaching and low-leaching groups. The slow phase varied widely among the subjects. There was no clear-cut relationship between half-time and type of particle. However, it seems probable that the slow phase was dependent on the degree of leaching, i.e., the half-times for elimination of intact particles from the lung are even slower. The large differences in long-term clearance among subjects indicate that long-term exposure to highly insoluble particles will result in large differences in lung burden. Subjects with a low capacity to eliminate alveolarly deposited particles are thus expected to be more susceptible to diseases in the alveolar part of the lung, i.e., diseases caused by certain insoluble particles.

Adult↗
PubMed1984

Lung morphology and phospholipids after experimental inhalation of soluble cadmium, copper, and cobalt.

Rabbits were exposed to chlorides of cadmium, copper, or cobalt, for 4-6 weeks (5 days/week and 6 hr/day) at levels ranging from 0.4 to 0.6 mg metal/m3. After exposure to Cd2+ the lungs were enlarged and an interstitial infiltration of neutrophils and lymphocytes as well as intraalveolar accumulations of large, vacuolated macrophages were observed. Morphometrical measurement of volume density of type II cells showed a 2.5-fold increase due to enhancement of cell size as well as cell number. The phospholipid content of lung tissue, determined in the lower left lobe, increased by 40%, mainly due to elevated levels of disaturated phosphatidylcholines. The results indicate that Cd2+ induces a reaction pattern similar to that seen following exposure to Ni2+, in addition to which Cd2+ causes interstitial alveolitis. Exposure to Cu2+ and Co2+ only affected the type II cells. Exposure to Cu2+ resulted in a 1.5-fold increase in volume density, probably due to enhanced number of cells. Following exposure to Co2+ the type II cells formed nodules protruding into the alveolar lumen. However, no significant increase in volume density occurred. The possible association between this abnormal growth pattern and early tumor formation deserves further investigation.

Aerosols↗
PubMed1984

Lysozyme levels in rabbit lung after inhalation of nickel, cadmium, cobalt, and copper chlorides.

Groups of rabbits were exposed to chlorides of nickel, cadmium, copper, and cobalt at concentrations ranging from 0.2 to 0.6 mg/m3 (as metal) for 4-6 weeks (5 days/week, 6 hr/day). Activity of lysozyme (muramidase) in lavage fluid, in alveolar macrophages, and in culture medium from macrophages incubated at 37 degrees C for 1 and 20 hr was estimated using the lyso-plate technique, agar plates with heat-killed Micrococcus lysodeikticus. In the nickel-exposed rabbits lysozyme activity in the mucous membrane from the left main bronchus was also estimated. Following nickel exposure the lysozyme level was significantly decreased in lavage fluid, macrophages, and in culture medium from incubated macrophages but remained unchanged in the mucous membrane. After exposure to cadmium, copper, and cobalt, lysozyme levels increased or were unchanged.

Animals↗
PubMed1984

Changes in glycerophosphatides and their ether analogs in lung lavage of rabbits exposed to nickel dust.

In rabbits exposed for 3 and 6 months to 1 mg/m3 of metallic nickel dust, the increase of pulmonary phospholipids was about 3 and 4 times, respectively. The corresponding increase of phospholipids in lung lavage was about 6 and 11 times, respectively. A detailed study of the phospholipid composition in lung lavage from the rabbits exposed for 3 months showed an increased amount of nonacidic phospholipids and a decreased amount of phosphatidylglycerols. Although most of the increase was due to the disaturated phosphatidylcholines, the relative increase was highest for the ether analogs of phosphatidylethanolamines. In the exposed rabbits the two ether analogs, 1-alk-1'-enyl-2-acyl- and 1-alkyl-2-acyl-sn-glycero-3-phosphoethanolamines, constituted 10.4 and 8.2%, respectively, of the phosphatidylethanolamine fraction. The corresponding values in the control rabbits were 5.2 and 0%, respectively. The occurrence of 1-alkyl-2-acyl-sn-glycero-3-phosphoethanolamines and the increase of 1-alk-1'-enyl-2-acyl-sn-glycero-3-phosphoenthanolamines indicate that the biosynthetic synthetic pathway of ether lipids may be stimulated in the exposed rabbits. This is of interest since a high proportion of ether lipids is observed in many tumors and since some nickel compounds may give respiratory tumors.

Animals↗
PubMed1984

Ability of rabbit alveolar macrophages to dissolve metals.

Manganese dioxide particles, 0.1-0.5 micron, were added to samples of 2-3 X 10(6) rabbit alveolar macrophages. The amount of manganese added and dissolved from the particles, over periods of 0, 1, 3, and 5 days, was determined by flame atomic absorption spectrophotometry. Macrophages from six rabbits received about 10 micrograms of Mn, macrophages from two rabbits about 30 micrograms, and macrophages from another two rabbits about 100 micrograms. Over periods of 1, 3, and 5 days the macrophages in all three dose groups dissolved two to three times more Mn than was dissolved in control experiments. In control experiments solubility was studied in the medium without macrophages. Macrophages cultivated 3 days before the addition of MnO2 dissolved the particles within another 2 days to an extent similar to that in the control experiments. The ability of the macrophages to dissolve MnO2 particles might be related to the low pH values in the phagosomes. Studies of the ability of macrophages from various species to dissolve metal particles as well as of pH values in their phagosomes might lead to a better understanding of alveolar clearance of metal particles.

Animals↗
PubMed1984

Airway resistance and deposition of particles in the lung.

The percentage 24-h lung retention of 4-micrometers monodispersed Teflon particles, aerodynamic diameter about 6 micrometers, was studied twice in 8 healthy nonsmokers. The particles were inhaled at 0.5 liter/sec with maximally deep breaths. Bronchoconstriction was induced by inhalation of a methacholine-bromide aerosol for one exposure before and for the other 20-30 min after the inhalation of the Teflon particles. For both exposures, airway resistance (Raw) was measured with a whole body plethysmograph before and after the induction of the bronchoconstriction and was found on an average to increase with a factor of 2-3. For the exposure when bronchoconstriction was induced after the inhalation of the Teflon particles, Raw and 24-h lung retention correlated significantly. Retention at 24 h was markedly lower when bronchoconstriction was induced before inhalation of the Teflon particles than when bronchoconstriction was induced after, the ranges being 13-24% and 38-68%, respectively. The experimental data agreed well with theoretical data from a lung model wherein the diameters of the airways were varied. The results indicate that the magnitude of bronchoconstriction occurring in real life can protect the alveolar part of the lung by reducing the amount of inhaled particles that deposit there.

Adult↗
PubMed1984

Toxicology of nickel.

Rabbits were exposed to low levels of airborne metals for 1-8 months, 5 days/week, 6 hours/day. After exposure, lung tissue was examined by light and electron microscopy. Macrophages lavaged from the left lung were examined morphologically and functionally. Phospholipids were analysed in lung tissue or lavage fluid. Metallic nickel dust, 0.1-1 mg/m3, affected alveolar macrophages, alveolar epithelial type II cells and phospholipids. In the lung tissue, nodular accumulation of macrophages was seen, and the volume density of alveolar type II cells was elevated. The amount of phospholipids was markedly increased, mainly due to an increase in disaturated phosphatidylcholines. After 1 month of exposure the macrophages appeared active. After 3 months they appeared 'overfed' and inactive. Metallic iron, chromium and cobalt did not produce the same effects as nickel. Exposure to 0.2 mg/m3 soluble nickel as nickel chloride produced almost identical effects to those of metallic nickel, indicating that the effect of the metallic nickel particles was caused by nickel ions. Exposure to cadmium chloride produced nearly all the effects produced by nickel chloride. However, cadmium chloride increased the level of lysozyme in the macrophages whereas nickel chloride decreased it. Cadmium chloride also produced interstitial alveolitis and cytoplasmic blebs on the surface of the macrophages. Cobalt chloride affected the growth of the type II cells, which formed nodules, but did not seem to affect the production of surfactant material by those cells. Copper chloride produced no effect apart from a slight increase in volume density of the type II cells. Thus, of four divalent metal ions, three (Ni2+, Cd2+ and Co2+) in similar concentrations in the inhaled air produced clear but different pathological effects in the lungs.

Animals↗
PubMed1983

Rabbit alveolar macrophages after inhalation of soluble cadmium, cobalt, and copper: a comparison with the effects of soluble nickel.

Rabbits were exposed to aerosols of chlorides of cadmium, copper, and cobalt (0.4-0.6 mg/m3 as metal) for 1 month (5 days/weeks and 6 hr/day). The effects of alveolar macrophages were compared with earlier reported effects of nickel chloride (0.3 mg/m3 as Ni). Effects of Cd2+ exposure resembled those of Ni2+ exposure. The number of macrophages in lavage fluid and the variance of cell diameters were thus increased and many cells contained lamellated inclusions. Contrary to macrophages from Ni2+-exposed rabbits, the surface of about 50% of the cells had cytoplasmic blebs. However, such cells were rarely seen by scanning electron microscopy. There were significantly more polymorphonucleated neutrophils and small lymphocytes, suggesting lung parenchymal damage. Cells from Cd2+-exposed animals, like cells from Ni2+-exposed ones, showed an increased oxidative metabolic activity after stimulation with Escherichia coli bacteria. Bactericidal capacity, on the other hand, tended to be enhanced rather than decreased, as in the nickel experiment. After CO2+ exposure, the number of macrophages was slightly increased in the lavage fluid and the cells showed an increased metabolic activity both at rest and upon stimulation with bacteria. Cu2+ exposure gave a slight increase in lamellated inclusions in the macrophages.

Aerosols↗