ABSTRACT
Three groups of five pigs were inoculated intratracheally with Escherichia coli lipopolysaccharides, and 24 hours later with 10 x 10(9) colony-forming units of a non-toxigenic strain of Pasteurella multocida type A; a fourth group was left uninoculated as controls. The three inoculated groups received either no treatment (positive controls), or were treated with 3 mg/kg ceftiofur intramuscularly once a day for five consecutive days, either alone or combined with 2 mg/kg flunixin intramuscularly once a day for three consecutive days. The sustained coughing and hyperthermia recorded in the positive controls disappeared after two days and three days of treatments, respectively, in the treated animals, and the reductions in daily weight gain and changes in breathing pattern observed in the controls were not observed in the treated animals. There were no significant differences between the pigs treated with ceftiofur alone or ceftiofur combined with flunixin. In the positive controls, the number of inflammatory cells in samples of bronchoalveolar lavage fluid continued to increase up to 15 days after inoculation, whereas in the treated animals there were similar increases at six days but the numbers had decreased to baseline levels after 15 days. Similarly, in the treated animals the volume of the lung lesions was significantly less than in the control animals, but the inclusion of flunixin in the treatment regimen had no significant additional effect.
Subject(s)
Anti-Bacterial Agents/therapeutic use , Anti-Inflammatory Agents, Non-Steroidal/therapeutic use , Bronchopneumonia/veterinary , Cephalosporins/therapeutic use , Clonixin/analogs & derivatives , Swine Diseases/drug therapy , Animals , Bronchopneumonia/drug therapy , Bronchopneumonia/microbiology , Clonixin/therapeutic use , Cough , Escherichia coli/pathogenicity , Escherichia coli Infections/drug therapy , Escherichia coli Infections/veterinary , Female , Lipopolysaccharides , Male , Pasteurella Infections/drug therapy , Pasteurella Infections/veterinary , Pasteurella multocida/pathogenicity , Swine , Swine Diseases/microbiology , Treatment OutcomeABSTRACT
The aim of this study was to investigate the role of particle number, total surface area, mass and surface chemical groups in (K(f,c)) changes. The lung effects of four different fine (110 nm) and ultrafine (24 nm) polystyrene particles have been tested in an isolated perfused rabbit lung model. Pulmonary microvascular permeability (K(f,c)) modifications were measured in response to intratracheal particle challenge. Polystyrene particles, mainly located in alveolar spaces and macrophages, induced a K(f,c) increase that was related to the total surface area and number of particles rather than to the instilled mass. Moreover, the positively charged amine-modified polystyrene particles were more effective in the K(f,c) response than the negatively charged carboxylate-modified polystyrene particles. We concluded that particle number and diameter that mathematically equally determined total surface area do not have the same importance in explaining the biological effects observed and that particle number could be an alternative to total surface area to describe the particle exposure. Furthermore, surface properties of polystyrene particles need to be considered to investigate the microvascular permeability changes measured in our model.
Subject(s)
Capillary Permeability/drug effects , Lung/blood supply , Microcirculation/drug effects , Polystyrenes/toxicity , Animals , In Vitro Techniques , Intubation, Intratracheal , Lung/pathology , Particle Size , Perfusion , Polystyrenes/administration & dosage , Rabbits , Surface PropertiesABSTRACT
The purpose of this work was to investigate the role of tachykinins in cough induced by citric acid (0.8 M) in pigs. With this object, we have studied the effect of citric acid on substance P content in the tracheo-bronchial tree and the effects of substance P and of tachykinin receptor antagonists on citric acid-induced cough. Citric acid exposure significantly increased substance P concentration in both broncho-alveolar and tracheal lavage fluids, while it decreased significantly the substance P content in tracheal mucosa. Substance P did not elicit cough, but significantly potentiated the citric acid-induced cough frequency. Tachykinin NK(1), NK(2) or NK(3) receptor antagonists, SR 140333 (nolpitantium), SR 48968 (saredutant) and SR 142801 (osanetant), respectively, significantly inhibited citric acid-induced cough. The same inhibitory effect of tachykinin receptor antagonists was observed, when substance P was nebulised before citric acid challenge. We conclude that citric acid induces in pigs a release of substance P in the tracheo-bronchial tree, which plays a sensitising role on the cough reflex. The involvement of tachykinin NK(1), NK(2), NK(3) receptors are also demonstrated in this reflex.
