Effects of oxygen exposure on it vitro function of pulmonary alveolar macrophages

Bacterial infection may complicate pulmonary oxygen (O2) toxicity, and animals exposed to high O2 concentrations show depressed in vivo pulmonary bacterial inactivation. Therefore, in vitro studies were undertaken to define the mechanism by which O2 alters pulmonary antibacterial activity. Normal and BCG pretreated rabbits were exposed to 100% O2 for 24, 48, and 72-h periods. Pulmonary alveolar macrophages (PAM) were obtained from the experimental animals and from nonoxygen exposed controls by bronchopulmonary lavage. O2 exposure did not alter cell yield or morphology. PAMs were suspended in 10% serum-buffer, and phagocytosis of (14C)Staphylococcus aureus 502A and (14C)Pseudomonas aeruginosa was measured. Comparison of the precent uptake of the 14C-labeled S. aureus after a 60-min incubation period demonstrated that normal PAMs exposed to O2 for 48 h showed a statistically significant increase in phagocytosis when compared to their controls (43.5 vs. 29.2%). A similar, but smaller increase was seen after 24-h O2 exposures. 48 and 72-h O2 exposures produced no significant changes in phagocytosis in PAMs from BCG-stimulated rabbits. Normal PAMs also showed an increased phagocytosis of Ps. aeruginosa after 48-h oxygen exposure. No impairment of in vitro bactericidal activity against either S. aureus 502A or Ps. aeruginosa could be demonstrated in PAMs from normal rabbits exposed to O2 for 48 h. These results indicate that the in vitrophagocytic and bactericidal capacity of the rabbit PAM is relatively resistant to the toxic effects of oxygen, and that imparied in vivo activity may possibly be mediated by effects other than irreversible metabolic damage to these cells. The mechanism for the observed stimulation of phagocytosis remains to be determined.     

Responses of alveolar macrophages and epithelial type II cells to oxidative DNA damage caused by paraquat

Naja kaouthia venom appeared in circulation rapidly after intramuscular injection into mice. The venom concentration attained a maximum level with all doses examined after 20 min. The half value of the maximum level was obtained 1 min after injection when a dose of 4LD50 was used. A critical venom concentration endangering mice was assessed from venom concentration in the sera of mice envenomed with sublethal dose (LD50). A fatal condition was produced within 30 min at a venom concentration of 200-300 ng/ml or within 50 min at a venom concentration of 100-150 ng/ml.     

Isolation and primary culture of murine alveolar type II cells

OBJECTIVES: The biotransformation of caffeine has been studied in vitro using human cytochrome P-450 isoenzymes (CYPs) expressed in human B-lymphoblastoid cell lines, namely CYP1A1, 1A2, 2A6, 2B6, 2D6-Val, 2E1 and 3A4, and microsomal epoxide hydroxylase (EH). In addition, CYP2D6-Met was also studied, in which a valine in the wild type (CYP2D6-Val) has been replaced by a methionine due to a G to A mutation in position 112. RESULTS: At caffeine 3 mmol center dot l-1, five CYPs (1A1, 1A2, 2D6-Met, 2E1 and 3A4) catalysed the biotransformation of caffeine. Among the enzymes studied, CYP1A2, which predominantly catalysed paraxanthine formation, had the highest intrinsic clearance (160 l center dot h-1 center dot mmol-1 CYP). Together with its high abundance in liver, it should be considered, therefore, to be the most important isoenzyme in caffeine metabolism. The affinity of caffeine for CYP1A1 was comparable to that of its homologue 1A2. CYP2D6-Met, which catalysed caffeine metabolism by demethylation and 8-hydroxylation, also had a relatively high intrinsic clearance (3.0 l center dot h-1 mmol-1 CYP), in particular for theophylline and paraxanthine formation, with kM values between 9-16 mmol center dot l-1. In contrast, the wild type, CYP2D6-Val, had no detectable activity. In comparison, CYP2E1 played a less important role in in vitro caffeine metabolism. CYP3A4 predominantly catalysed 8-hydroxylation with a kM value of 46 mmol center dot l-1 and an intrinsic clearance of 0.60 l center dot h-1 center dot mmol-1 CYP. Due to its high abundance in human liver, the latter CYP may contribute significantly to the in vivo formation of TMU. CONCLUSION: The findings of this study indicate that i) microsomes from transfected human B-lymphoblastoid cell lines give results close to those obtained with microsomes isolated from human liver, ii) at least four CYP isoforms are involved in caffeine metabolism, iii) at a substrate concentration <0.1 mmol center dot l-1, CYP1A2 and 1A1 are the most important isoenzymes, iv) at higher concentrations the participation of other isoenzymes, in particular CYP3A4, 2E1 and possibly also CYP2D6-Met, are important in caffeine metabolism, and v) the nucleotide composition at position 1120 of CYP2D6 determines the activity of this isoenzyme in caffeine metabolism.     

Tumor necrosis factor-alpha induces emphysema-like pulmonary tissue rebuilding. Changes in type II alveolar epithelial cells

This study has investigated the relative involvement of cholinergic, adrenergic, nitric oxide and tachykininergic transmission in extrinsic neural influences on the lower oesophageal sphincter (LOS) in urethane anaesthetized ferrets. A micromanometric assembly (OD 1.75 mm) incorporating a sleeve sensor was used for high-fidelity oesophageal, LOS and gastric pressure measurement at low perfusion rates (< 0.1 ml/min). The LOS response to vagal and splanchnic nerve stimulation (0.5 ms pulse width, 10 s duration) was frequency- and voltage-dependent. LOS responses to stimulation at 20 V, 10 Hz were investigated in separate groups of animals with either L-NAME (100 mg/kg), hexamethonium (15 mg/kg), guanethidine (5 mg/kg), CP96,345 (NK-1 antagonist, 4 mg/kg), atropine (0.4 mg/kg) or propranolol (1 mg/kg). Propranolol treatment was followed by yohimbine (1 mg/kg) and prazosin (0.25 mg/kg). Vagal stimulation caused an immediate decrease in LOS pressure, followed by increase on cessation of stimulation, followed by a prolonged decrease (77 +/- 2%) for up to 5 min. L-NAME did not affect inhibition, but increased excitation 4-fold (p < 0.001). Guanethidine and CP96,345 had no major effect. Hexamethonium decreased the inhibitory (p < 0.05) and excitatory (p < 0.01) responses. Atropine reduced the excitatory response (p < 0.05). Some inhibition still remained if all treatments were combined. Splanchnic stimulation reduced LOS pressure by 70 +/- 6% for 101 +/- 17 s. L-NAME, guanethidine, hexamethonium and CP96,345 all independently significantly reduced inhibition. The combination of guanethidine and CP96,345 usually abolished splanchnic-induced inhibition. Atropine was without effect. Propranolol (1 mg/kg) changed the splanchnic-induced response from mainly inhibition to excitation (100 +/- 44% increase). LOS responses to noradrenaline (1-10 micrograms close IA) showed similar features to responses to splanchnic stimulation. We conclude that vagal stimulation evokes LOS relaxation via activation of established cholinergic and NANC mechanisms and other, unidentified mechanisms. Splanchnic stimulation activates adrenergic neurones probably via nicotinic and non-nicotinic ganglionic mechanisms, which in turn elicit beta adrenergic inhibitory effects on the LOS. Splanchnic stimulation also antidromically activates spinal afferent fibres. These may release substance P from peripheral myenteric plexus and prevertebral ganglionic endings causing activation of myenteric NANC inhibitory neurones and sympathetic neurones, respectively.     

E1A-induced immortalization of rat type II alveolar epithelial cells

Using a retroviral vector expressing the adenoviral 12S E1A gene product the authors have immortalized rat type II alveolar epithelial cells. For a period of time, the immortalized cells retain many of the ultrastructural characteristics of type II cells in situ, including the presence of lamellar bodies. By 250 days in culture, however, neither lamellar bodies, SP-A, nor a phospholipid profile characteristic of surfactant were present. The cell bind the lectin Maclura pomifera and stably express cytokeratins and the E1A gene product. The cell line also has a diploid karyotype, exhibits contact inhibition of growth, and does not grow in soft agar. E1A-immortalized cell lines should prove useful as models for study of certain aspects of type II alveolar epithelial cell function.     

Cyclophosphamide-induced generation of reactive oxygen species. Comparison with morphological changes in type II alveolar epithelial cells and lung capillaries

Immunosenescence involves modifications of humoral and cellular immunity. Here we report the analysis of human leukocyte antigen (HLA) expression on T lymphocytes, B lymphocytes and monocytes of 58 healthy subjects aged 23-95 years old. Using a double staining immunofluorescence and flow cytometry analysis, we have determined the percentages of cells expressing HLA class-I and HLA-DR antigens. The number of antigenic sites expressed per cell were evaluated for HLA-ABCw, HLA-A, HLA-B, HLA-DR locus with a flow cytometry quantification technique. With advancing age, we observed: (i) a significant decrease of the percentage of T cells and B cells expressing HLA-A products; (ii) a decrease of the number of HLA class-I antigenic sites expressed per cell on the three populations tested, predominantly on B cells and in a locus-dependent fashion; (iii) a decrease of the number of HLA-DR molecules expressed per T cell, although the percentage of T cells expressing DR products was increased; (iv) a significant diminution of the percentage of B cells expressing HLA-DR molecules, without changes of the number of HLA-DR antigenic sites per cells. These changes in HLA expression with increasing age could contribute to the decreased level of immunologic responsiveness observed with ageing and contribute to the modification of antigen recognition.     

Type II alveolar epithelial cells and free alveolar cells after intratumor TNF-alpha administration

The experiment used Morris hepatoma 5123 series growing in muscles of the Buffalo rats. A suspension of 3 x 10(6) neoplastic cells was injected into the right hind leg of the animals. After fourteen days, TNF-alpha was administered into the tumour in a dose of 1.5 x 10(4) U/24 hours in 0.5 ml PBS solution. The group I animals were injected for 4 days and group II for 8 days. Control groups consisted of rats with injected Morris hepatoma which were given PBS solution instead of TNF-alpha (group III A and B) and animals without the hepatoma, given 4 or 8 TNF-alpha, respectively (groups IV A and B). In the present study, we have explored the effect of intratumor TNF-alpha administration on the composition of cells isolated from the lungs through multiple bronchoalveolar lavages (BAL). Ultrastructural evaluation of the pulmonary tissue was done using a transmission electron microscope (TEM), with special attention paid to type II alveolar epithelial cells and free alveolar cells. Examinations in TEM in groups I, II and IV (A and B) found, in the lumen of alveoli, an increase in the number of alveolar macrophages (AM) with morphological features of intensified activity and AM with numerous secondary lysosomes containing material of phospholipid structure. Also, numerous type II alveolar epithelial cells with emptied lamellar bodies were observed. The above mentioned changes were especially marked after eightfold TNF-alpha administration. In groups I, II and IV (A and B), compared with group III, a significant increase was found in the total number of cells isolated by BAL as well as in the number of cells with positive reaction in staining according to Beckstead's method. It may indicate that the changes in the parameters mentioned above are related to TNF-alpha action. The results obtained indicate the possibility of systemic effect of TNF-alpha after its administration into the experimental Morris hepatoma.     

Oxidative inactivation of alpha 1-proteinase inhibitor by alveolar epithelial type II cells

The aim of this work was to evaluate the ability of guinea pig alveolar epithelial type II cells to generate significant amounts of reactive oxygen species to inactivate alpha 1-proteinase inhibitor (alpha 1-PI). Inactivation of alpha 1-PI was evaluated by its inhibitory activity against porcine pancreatic elastase and was expressed as a percentage. The same experiments were performed in parallel with alveolar macrophages (AM) obtained from the same animals and with MRC-5 fibroblasts. Both type II cells and AM released significant amounts of hydrogen peroxide and superoxide, whereas the fibroblasts did not. Unstimulated type II cells (0.5 +/- 2%), AM (1.2 +/- 1.5%), and fibroblasts (0.5 +/- 0.5%) were unable to inactivate alpha 1-PI. Addition of phorbol myristate acetate did not increase their ability to inactivate alpha 1-PI. In contrast, type II cells (79.7 +/- 7%) and AM (80.1 +/- 8%) dramatically inactivated alpha 1-PI in the presence of myeloperoxidase (25 mU/ml), whereas fibroblasts did not. Addition of catalase to the reaction significantly prevented the inactivation of alpha 1-PI. Western blot analysis of alpha 1-PI did not reveal a significant proteolysis of alpha 1-PI, which supports the hypothesis that, in the presence of neutrophil-derived myeloperoxidase, type II cells may oxidatively inactivate alpha 1-PI.     

Dynamics of surfactant release in alveolar type II cells

Pulmonary surfactant, secreted via exocytosis of lamellar bodies (LB) by alveolar type II (AT II) cells, maintains low alveolar surface tension and is therefore essential for normal lung function. Here we describe real-time monitoring of exocytotic activity in these cells by visualizing and quantifying LB fusion with the plasma membrane (PM). Two approaches were used. First, fluorescence of LysoTracker Green DND-26 (LTG) in LB disappeared when the dye was released after exocytosis. Second, phospholipid staining by FM 1-43 resulted in bright fluorescence when this dye entered the LB through the fusion pore. Both processes were restricted to and colocalized with LB and occurred simultaneously. In AT II cells, FM 1-43 offered the unique advantage to independently define the moment and cellular location of single exocytotic events as well as the amount of material released, and to monitor its extracellular fate. Furthermore, both dyes could be used in combination with fura-2. The results indicate considerable diversity in the dynamics of LB exocytosis. In the majority of cells stimulated with ATP and isoproterenol, the first fusion of LB coincided with the rise of [Ca2+]i, but subsequent response of other LB in the same cell considerably outlasted this signal. In other cells, however, the onset of exocytosis was delayed by several minutes. After LB fusion, release of surfactant from LB into an aqueous solution was slow. In summary, stimulated exocytosis in AT II cells occurs at a much slower rate than in most other secretory cells but is still a more dynamic process than predicted from conventional measurements of surfactant released into cell supernatants.     

Inducible expression of the alpha1-acid glycoprotein by rat and human type II alveolar epithelial cells

Alpha1-acid glycoprotein (AGP) is a major acute phase protein in rat and human. AGP has important immunomodulatory functions that are potentially important for pulmonary inflammatory response. The liver is the main tissue for AGP synthesis in the organism, but the expression of AGP in the rat lung has not been investigated. We show that AGP mRNA was induced in the lung of dexamethasone-, turpentine-, or LPS-treated rats, whereas AGP mRNA was not detected in the lung of control rats. In the lung of animals treated intratracheally with LPS, in situ hybridization showed that AGP gene expression was restricted to cells located in the corners of the alveolus, consistent with an alveolar type II (ATII) cell localization. The inducible expression of the AGP gene was confirmed in vitro with SV40 T2 cells and rat ATII cells in primary culture: maximal expression required the presence of dexamethasone. IL-1 and the conditioned medium of alveolar macrophages acted synergistically with dexamethasone. Rat ATII cells secreted immunoreactive AGP in vitro when stimulated with dexamethasone or with a combination of dexamethasone and the conditioned medium of alveolar macrophages. In vivo, in the human lung, we detected immunoreactive AGP in hyperplastic ATII cells, whereas we did not detect AGP in the normal lung. We conclude that AGP is expressed in the lung in cases of inflammation and that ATII cells are the main source of AGP in the lung.     

Effect of time in culture on modulation of Na(+)-K(+)-ATPase activity in rat alveolar type II cells

To determine the effect of time in culture on epithelial cell function, we evaluated the modulation of Na(+)-K(+)-ATPase activity in rat alveolar type II cells in culture. Ouabain sensitivity testing revealed that the alpha-1 predominance in the enzyme's isoforms was maintained over the 120 hours in culture. Basal Na(+)-K(+)-ATPase activity in the whole cell homogenate did not differ significantly between cells cultured for 48 hours and those cultured for 120 hours. Terbutaline (10 mM) did not activate Na(+)-K(+)-ATPase in the cells cultured for 48 hours, but, it significantly increased the activity of this enzyme in the cells cultured for 120 hours cells cultured for 48 hours, produced intracellular cyclic AMP after exposure to 10 mM of terbutaline. These results indicate that the coupling between Na(+)-K(+)-ATPase and the beta-adrenergic pathway in alveolar type II cells can be influenced by the time in cell culture.     

Effects of erythromycin on surfactant synthesis, secretion, and recycling by rat alveolar type II cells

Effects of erythromycin on surfactant synthesis, secretion, and recycling by rat alveolar type II cells were examined. Type II cells were isolated from rat lungs and incubated with 3H-choline, a precursor of surfactant. Synthesis was quantified from the amount of 3H-phosphatidylcholine and from the distribution to lamellar body fractions as measured with sucrose density gradients. Secretion was quantified from the percent of synthesized 3H-phosphatidylcholine released into the medium over 3 hr. Recycling was quantified from the percent uptake over 1 h of 3H-labeled synthetic liposomes. Type II cells incubated with erythromycin (5-50 micrograms/ml) for 22 hrs secreted less surfactant in response to PMA and ATP than did control cells. Erythromycin did not affect synthesis or recycling of surfactant by type II cells. These results show that erythromycin inhibits surfactant secretion from type II cells, and suggest that erythromycin may be effective in surfactant-excess states such as alveolar proteinosis.     

Mycobacterium tuberculosis invades and replicates within type II alveolar cells

Although Mycobacterium tuberculosis is assumed to infect primarily alveolar macrophages after being aspirated into the lung in aerosol form, it is plausible to hypothesize that M. tuberculosis can come in contact with alveolar epithelial cells upon arrival into the alveolar space. Therefore, as a first step toward investigation of the interaction between M. tuberculosis and alveolar epithelial cells, we examined the ability of M. tuberculosis to bind to and invade alveolar epithelial cells in vitro. The H37Rv and H37Ra strains of M. tuberculosis were cultured to mid-log phase and used in both adherence and invasion assays. The A549 human type II alveolar cell line was cultured to confluence in RPMI 1640 supplemented with 5% fetal bovine serum, L-glutamine, and nonessential amino acids. H37Rv was more efficient in entering A549 cells than H37Ra, Mycobacterium avium, and Escherichia coli Hb101, and nonpiliated strain (4.7% +/- 1.0% of the initial inoculum in 2 h compared with 3.1% +/- 0.8%, 2.1% +/- 0.9%, and 0.03% +/- 0.0%, respectively). The invasion was more efficient at 37 degrees C than 30 degrees C (4.7% +/- 1.0% compared with 2.3% +/- 0.8%). H37Rv and H37Ra were both capable of multiplying intracellularly at a similar ration over 4 days. Binding was inhibited up to 55.7% by anti-CD51 antibody (antivitronectin receptor), up to 55% with anti-CD29 antibody (beta(1) integrin), and 79% with both antibodies used together. Update of M. tuberculosis H37Rv was microtubule and microfilament dependent. It was inhibited by 6l.4% in the presence of 10 micron colchicine and by 72.3% in the presence of 3 micron cytochalasin D, suggesting two separate pathways for uptake. Our results show that M. tuberculosis is capable of invading type II alveolar epithelial cells and raise the possibility that invasion of alveolar epithelial cells is associated with the pathogenesis of lung infection.     

Apoptosis in macrophages and alveolar epithelial cells during early stages of infection by Legionella pneumophila and its role in cytopathogenicity

The hallmark of Legionnaires' disease is intracellular replication of Legionella pneumophila within cells in the alveolar spaces. Cytopathogenicity of this bacterium to the host cell has been well demonstrated, but the mechanisms of host cell death due to infection by L. pneumophila are not well understood. In this study, induction of apoptosis in macrophages and alveolar epithelial cells by L. pneumophila during early stages of infection was confirmed by using multiple criteria, including DNA fragmentation by agarose gel electrophoresis, terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling, surface exposure of phosphatidylserine, and cellular morphology by transmission electron microscopy. Induction of nuclear apoptosis in L. pneumophila-infected macrophages is mediated by activation of the caspase cascade death machinery. We provide genetic and biochemical evidence that L. pneumophila-induced apoptosis in macrophages and alveolar epithelial cells does not require intracellular bacterial replication or new protein synthesis. In addition, extracellular L. pneumophila is capable of inducing apoptosis. Furthermore, induction of apoptosis by L. pneumophila correlates with cytopathogenicity. We conclude that L. pneumophila-induced apoptosis in macrophages and alveolar epithelial cells plays an important role in cytopathogenicity to the host cell during early stages of infection.     

Enhancing effects of the supernatant of pulmonary alveolar macrophages stimulated by BCG on proliferation on pulmonary fibroblasts

The supernatant of pulmonary alveolar macrophages (PAM) stimulated by 7.5-60mg/L of BCG could significantly enhance proliferation of pulmonary fibroblasts (PFB), and the supernatant contained high level of TNF. This result indicated BCG could stimulate PAM to produce TNF in vitro. On the other hand, the supernatant of PAM stimulated by 50mg/L of SiO2 could also enhance proliferation of PFB, but the level of TNF in the supernatant was very low and it demonstrated the ingredient in the supernatant enhancing proliferation was not TNF. TNF showed synergistic effect with this ingredient for enhancing proliferation of PFB. Therefore, TNF produced by tuberculosis bacteria-stimulated PAM might be an important factor enhancing the development of fibrosis of silicotuberculosis.     

Nitric oxide production following in vitro stimulation of ovine pulmonary alveolar macrophages

A large-scale study was undertaken to investigate the effects of two systematic anthelmintic treatments on village cattle productivity in the Gambia. Treated animals had significantly higher performance in terms of live weights and age at first calving, but the mortality rate of 0- to 1-yr-old cattle appeared to be negatively affected. These results and financial data on treatment costs were used in a herd simulation model to assess the profitability of the intervention. Treatment was profitable on average, but the risks of losing money were large and average returns were sensitive to various hypotheses examined. The treatment regimen studied can only be recommended in certain herds and further research is needed to identify the factors determining the negative response in other herds.     

Trafficking of newly synthesized surfactant protein A in isolated rat alveolar type II cells

We examined the synthesis, transport, and localization of surfactant protein A (SP-A) in primary cultures of alveolar type II cells. In type II cells maintained in culture for 6 h, 39% of the SP-A pool detected with an enzyme-linked immunosorbent assay (ELISA) was found in lamellar bodies (LBs). After 24 h in culture, 53% of the cellular SP-A pool was found in LBs. The absolute amount of SP-A in the LB compartment was almost identical at 6 and 24 h of culture. In contrast to the results obtained with ELISA, 35S labeling of newly synthesized SP-A revealed that less than 7% of the cellular SP-A pool was in LBs at either 6 or 24 h of culture. In the 6-h cultures, 17% of the total (i.e., cells and media) [35S]SP-A pool was extracellular. In the 24-h cultures, 70% of the [35S]SP-A pool was extracellular. The secretion of [35S]SP-A was blocked by brefeldin A at all times. When medium containing newly secreted [35S]SP-A was incubated with alveolar type II cells maintained in culture for 24 h, the protein was taken up and incorporated into the LB fraction. More than 80% of the internalized SP-A was associated with the LB compartment after a 6 h incubation. The uptake of [35S]SP-A was blocked at 4 degrees C and was promoted by addition of unlabeled SP-A at 37 degrees C. These findings support a pathway of extracellular routing of SP-A prior to its accumulation in LBs in cultured type II cells.     

Adult alveolar type II cells lack cAMP and Ca(2+)-activated Cl-channels

The recently developed procedure of chromosomal DNA loop excision by topoisomerase II-mediated DNA cleavage at matrix attachment sites (S. V. Razin, R. Hancock, O. Iarovaia, O. Westergaard, I. Gromova, and G. P. Georgiev, Cold Spring Harbor Symp. Quant. Biol. 58:25-35, 1993; I. I. Gromova, B. Thompsen, and S. V. Razin, Proc. Natl. Acad. Sci. USA 92:102-106, 1995) has been employed for mapping the DNA loop anchorage sites in a 500-kb region of the Drosophila melanogaster X chromosome. Eleven anchorage sites delimiting 10 DNA loops ranging in size from 20 to 90 kb were found within this region. Ten of these 11 anchorage sites colocalize with previously mapped scaffold attachment regions. However, a number of other scaffold attachment regions are found to be located in loop DNA.     

Influence of beta-endorphin on the production of reactive oxygen and nitrogen intermediates by rabbit alveolar macrophages

We have compared the cuffed oropharyngeal airway (COPA), a modified Guedel airway device with a specially designed cuff at its distal end, with the laryngeal mask airway (LMA), on haemodynamic and electroencephalographic (EEG) responses to insertion. In addition, we examined the haemodynamic and EEG changes during initiation of the effect-compartment controlled infusion. We studied 35 female patients undergoing ambulatory gynaecological surgery allocated randomly to received an LMA or COPA to manage the airway. After premedication with midazolam 0.03 mg kg-1 i.v. and low-dose alfentanil (0.01 mg kg-1), anaesthesia was induced and maintained with propofol, using an effect-compartment controlled infusion set at an effect-site concentration of 4 micrograms ml-1. After intercompartmental equilibration, the LMA (group I) or COPA (group II) was inserted and haemodynamic (arterial pressure, heart rate) and EEG (bispectral index (BIS)) responses to insertion studied. The effect-compartment controlled infusion of propofol caused only mild haemodynamic changes during induction. Changes in arterial pressure and heart rate after insertion were similar in both groups and not significantly different from baseline values before insertion. Changes in BIS after insertion were minor and similar between groups.     

Effect of chrysotile-asbestos and zeolites dust on generations of reactive oxygen species by alveolar macrophages and granulocytes

OBJECTIVE: To evaluate the discrepancy index between the clinical and histological diagnosis and the prevalence of epithelial dysplasia and carcinoma in 45 patients with potentially malignant epithelial oral lesions (PMEL). PATIENTS AND METHODS: We submitted 45 patients with PMEL to clinical examination and obtained a biopsy from each. The results of histological diagnosis were compared to the clinical diagnosis. RESULTS: Clinical diagnosis showed that the most common PMEL was leukoplakia followed by lichen planus and by actinic cheilitis associated with leukoplakia. The most common site was the buccal mucosa. Histological diagnosis revealed that 46.7% of the PMEL were lichen planus. The discrepancy index between clinical and histological diagnosis was 24.4%. The higher discrepancy index occurred among leukoplakias. The prevalence of epithelial dysplasia and carcinoma was 17.8%. CONCLUSIONS: We conclude that all PMEL should be submitted to a microscopic analysis because the discrepancy between clinical and histological diagnosis was present in a quarter of these lesions. Otherwise, the epithelial dysplasia and carcinoma were more frequent in the leukoplakias.