Background: Several lung diseases are characterized by a predominantly neutrophilic inflammation. A better understanding of the mechanisms of action of some drugs on the airway inflammation of such diseases may bring advances to the treatment. Objective: To develop a method to induce pulmonary neutrophilic response in mice, without active infection. Methods: Eight adult Swiss mice were used. The study group (n = 4) received an intranasal challenge with 1 x 1012 CFU/ml of Pseudomonas aeruginosa (Psa), frozen to death. The control group (n = 4) received an intranasal challenge with saline solution. Two days after the intranasal challenge, a bronchoalveolar lavage (BAL) was performed with total cell and differential cellularity counts. Results: The total cell count was significantly higher in the group with Psa, as compared to the control group (median of 1.17 x 106 and 0.08 x 106, respectively, p = 0.029). In addition to this, an absolute predominance of neutrophils was found in the differential cellularity of the mice that had received the Psa challenge. Conclusion: The model of inducing a neutrophilic pulmonary disease using frost-dead bacteria was successfully developed. This neutrophilic inflammatory response induction model in Swiss mice lungs may be an important tool for testing the anti-inflammatory effect of some antimicrobial drugs on the inflammation of the lower airways.

Keywords: Animal experimentation. Lung disesases. Inflammation. Neutrophils. Pseudomonas.

Objective: To determine whether pulmonary mechanics are altered in mice with sepsis. Methods: A total of 40 Balb/c mice were divided into two groups: survival (n = 21) and pulmonary mechanics (n = 19). The survival group was divided into three subgroups: control (n = 7), sublethal (n = 7) and lethal (n = 7). The pulmonary mechanics group was also divided into three subgroups: control (n = 5), sublethal (n = 7) and lethal (n = 7). Sepsis was induced through cecal ligation and puncture, the latter varying in degree (sublethal or lethal). At eight hours after the intervention, pulmonary mechanics were measured through end-inflation occlusion. In the pulmonary mechanics group, the following variables were studied: total pressure, resistance, viscoelasticity, dynamic compliance and static compliance. The data obtained were analyzed using one-way ANOVA. Results: The data for the survival group indicate the efficacy of the model employed. There were no statistically significant differences among the pulmonary mechanics subgroups in terms of dynamic compliance, static compliance, total pressure, resistance or viscoelasticity. Conclusion: At eight hours after cecal ligation and puncture, there were no changes in the lung parenchyma, nor were any alterations observed in the viscous and viscoelastic components of the lung.

Keywords: Sepsis; Respiratory mechanics; Lung/injuries; Punctures/instrumentation; Respiratory distress syndrome, adult; Mice

Objective: To determine whether a short-term protocol using subcutaneous sensitization with ovalbumin, without the use of adjuvants, would induce an eosinophilic response in the lungs of mice similar to that observed in previous, well-established protocols. Methods: Adult female BALB/c mice were randomized and divided into groups according to the number of sensitizations with ovalbumin and the number/dosage of intranasal ovalbumin challenges. The short-term protocol (10 days) consisted of one sensitization with ovalbumin and three ovalbumin challenges (100 µg). Total and differential cell counts in BAL fluid, levels of eosinophil peroxidase in lung tissue, and histopathological examination of the lungs were performed 24 h after the last ovalbumin challenge. Results: No significant differences were found among the groups regarding the variables studied. The short-term protocol, as well as the other protocols studied, induced an eosinophilic response similar to that obtained in the positive control. Conclusions: Subcutaneous sensitization with ovalbumin and without the use of adjuvants resulted in a significant allergic response in the lungs of mice, even in the short-term protocol group. Our findings suggest that this short-term protocol can be used as a first-line pre-clinical test for the study of new medications, reducing the costs and observation periods.

Keywords: Ovalbumin; Mice; Asthma.

Background: Structural alterations to the pulmonary circulation characterize the vascular remodeling process and are likely correlated with local variations in flow and ischemia. Objective: To define the histological alterations to the pulmonary circulation seen after experimentally-induced ischemia of the pulmonary artery and to correlate those alterations with known patterns of blood redistribution and vascular remodeling. Method: Wistar rats (n = 48) were randomized into two groups with ligation of the pulmonary artery and without (controls) and were sacrificed on post-ischemia days 1, 7, 30 and 60. Lungs were removed and inspected for signs of parenchymal injury. External diameters, as well as wall thicknesses in the pulmonary, alveolar and bronchial end arterioles, were measured. Internal diameter and wall thickness percentage were calculated. Results: Infarction, necrosis and hemorrhage occurred only in ischemic lungs. In nonischemic lungs, there was a sustained increase in the internal and external arteriolar diameters, with an initial reduction in wall thickness on day 1, and day-60 values were similar to those seen in controls. In ischemic lungs, there was a transitory reduction in the internal and external diameters of the pulmonary and bronchial end arterioles, together with an initial, equally transitory, increase in their wall thickness. The alveolar arterioles presented sustained and progressive increases in external diameter and wall thickness, with concomitant reductions in internal diameter. Conclusion: This model mimics distal arterial disease in patients with chronic pulmonary thromboembolism. The vascular response in nonischemic lungs was consistent with a pattern of flow remodeling, whereas that seen in ischemic lungs was more consistent with flow and ischemia. In the pulmonary and bronchial end arterioles, the response was transitory, in contrast to the sustained and progressive response seen in the alveolar arterioles, which was probably caused by delayed local flow.

Keywords: Key-words: Pulmonary embolism. Pulmonary circulation. Vascular remodelling. Pulmonary artery.

Objective: To describe the development of a silicone stent and perform in vivo testing for biocompatibility/applicability in the normal canine trachea. Methods: Four different densities were tested in order to obtain the silicone prototypes. The pressure required for compression considering a contact area of 1 cm2, and a 30% reduction in diameter was calculated for each density. The best density was 70-75 Shore A hardness. Powdered barium sulfate was added to the silicone to make the stent radiopaque and easily identifiable in radiological imaging. This novel stent presents a corrugated external surface with discontinuous and protruding arcs resembling the tracheobronchial rings (for intercalation and fixation in the lumen of the lower airways), a highly polished inner surface and smooth extremities (to prevent friction-related damage). The prototype considered most appropriate in terms of rigidity and flexibility was bronchoscopically implanted in normal canine tracheas. After eight weeks, the animals were euthanized, and the tracheas were removed for anatomopathological analysis. Results: There were no postimplantation complications, and none had to be removed. After eight weeks, the devices were found to be well-positioned. Histopathology revealed a well-preserved epithelial basal membrane, foci of denuded epithelium, mild submucosal inflammatory infiltrate with scattered granulation tissue, vascular neoformation, and no microorganisms. Conclusions: The stent developed proved resistant to mechanical stress, biocompatible in the canine trachea and well-preserved at the study endpoint.

Keywords: Implants, experimental; Silicones; Biocompatible materials.

We aimed to test a new model of self-expanding tracheal stent so that it might be made available for clinical use. Using direct laryngoscopy, we placed polyurethane-coated, nitinol stents into the middle third of the trachea in 25 New Zealand rabbits. After a mean observation period of 26 days, we evaluated stent migration, degree of expansion, attachment, adherence, formation of granulation tissue, presence of inflammatory infiltrate, parietal involvement, and epithelial lining. The results showed complete radial expansion, little adherence to the tracheal mucosa, and low tissue attachment, as well as high rates of granuloma formation and stent migration. This new model proved to be biocompatible and showed a behavior similar to that of other stents on the market.

Keywords: Prosthesis implantation; Tracheal stenosis; Rabbits; Stents.

Background: Lung volume reduction surgery may be a viable treatment alternative for emphysema patients suffering from severe respiratory insufficiency. Objectives: To evaluate functional and morphological aspects of emphysematous rat lungs, prior to and following lung volume reduction surgery. Method: Wistar rats were divided into two experimental groups (papain without surgery and papain with surgery) and three control groups (saline without surgery, saline with surgery and papain without mechanical ventilation). After approximately 40 days of endotracheal instillation of papain or saline solution, animals in the papain with surgery and saline with surgery groups were submitted to bilobectomy of the middle lobes by right thoracotomy along the posterior border of the superior vena cava. After 1 week, the same animals were submitted to a mechanical ventilation study, which involved measurement of lung elasticity and airway resistance. For all of the animals studied, lung tissue was analyzed in order to determine alveolar diameter and the elastic fiber quantity. Results: Morphometric analysis revealed higher mean alveolar diameter in the lungs of all animals exposed to papain as compared to those exposed to saline. Elastic fiber counts in the alveolar septa of animals treated with papain were lower than those of animals receiving saline. In the animals submitted to bilobectomy and papain, lung elasticity was greater than in those receiving papain without surgery and was statistically equal to that seen in animals receiving saline (with or without surgery). Conclusion: In the respiratory systems of animals with pulmonary emphysema submitted to lung volume reduction by bilobectomy, the capacity for elastic recoil returned to values equivalent to those of the control group animals.

Keywords: Key words: Pulmonary emphysema. Papain/drugs efects. Case-control studies. Disease models, animal. Respiratory mechanics/drugs efects. Lung/sugery. Lung/anatomy & histology.

Objective: Brain death (BD) triggers important hemodynamic and inflammatory alterations, compromising the viability of organs suitable for transplantation. To better understand the mi-crocirculatory alterations in donor lungs caused by BD. The present study investigated the pul-monary microcirculation in a rodent model of BD via intravital microscopy. Methods: Male Wistar rats were anaesthetized and mechanically ventilated. They were trepanned and BD was induced through the increase in intracranial pressure. As control group, sham-operated (SH) rats were trepanned only. In both groups, expiratory O2 and CO2 were monitored and after three hours, a thoracotomy was performed, and a window was created to observe the lung surface using an epi-fluorescence intravital microscopy. Lung expression of intercellular adhesion molecule (ICAM)-1 and endothelial nitric oxide synthase (eNOS) was evaluated by immunohistochemistry, and cytokines were measured in lung samples. Results: Three hours after the surgical proce-dures, pulmonary perfusion was 73% in the SH group. On the other hand, BD animals showed an important decrease in organ perfusion to 28% (p = 0.036). Lung microcirculatory compromise after BD induction was associated with an augmentation of the number of leukocytes recruited to lung tissue, and with a reduction in eNOS expression and an increase in ICAM-1 expression on lung endothelial cells. BD rats showed higher values of expiratory O2 and lower values of CO2 in comparison with SH animals after three hours of monitoring. Conclusion: Data presented showed that BD triggers an important hypoperfusion and inflammation in the lungs, compromis-ing the donor pulmonary microcirculation

Keywords: Brain death; Inflammation; Intravital microscopy; Lung microcirculation.

Objective: To evaluate the pulmonary alterations of animals with Hepatopulmonary Syndrome (HPS) submitted to Biliary Duct Ligature (BDL), as well as the antioxidant effect of Melatonin (MEL). Methods: Sixteen male Wistar rats, divided into four Sham groups: BDL group, Sham + MEL group and BDL + MEL. The pulmonary and hepatic histology, lipoperoxidation and antioxidant activity of lung tissue, alveolar-arterial O2 difference and lung / body weight ratio (%) were evaluated. Results: When comparing the groups, could be observed an increase of vasodilation and pulmonary fibrosis in the BDL group and the reduction of this in relation to the BDL + MEL group. It was also observed significant changes in the activity of catalase, ApCO2, ApO2 in the LBD group when compared to the other groups. Conclusion: The use of MEL has been shown to be effective in reducing vasodilation, fibrosis levels and oxidative stress as well as gas exchange in an experimental HPS model.

Keywords: Bile duct; Hepatopulmonary Syndrome; Melatonin; Lung.

Objective: The reproduction of an experimental emphysema model in rats by intratracheal instillation of papain was proposed for the evaluation of lung volume reduction surgeries. Method: The study used orotracheal instillation of papain (20 mg/kg) dissolved in 0.9% saline solution. Forty days after instillation, animals underwent mechanical ventilation. Elastance and resistance of the respiratory system were measured, and the rats were sacrificed by having their lungs removed. The pulmonary tissue of the animals was qualitatively analyzed with hematoxylineosin staining and submitted to morphometric analysis for the measurement of the mean alveolar diameter. The pulmonary tissue was also subjected to resorcin-fuchsin staining for the identification of elastic fibers, which were quantified in alveolar septa by digital imaging. Results: In the animals instilled with papain, the histological analysis of the lungs showed pan-acinar emphysema, with rupture of alveolar septa and hyperdistention. Morphometric analysis showed higher mean values for mean alveolar diameter in the lungs of the animals submitted to papain (149.08 μm and 100.56 μm) as compared to the group receiving saline solution (64.08 μm and 75.90 μm). The quantification of elastic fibers of alveolar septa of papain-treated animals was 70% lower than in the animals receiving saline solution. Mechanic ventilation did not show differences in respiratory system resistance of animals receiving papain or saline solution. Respiratory system elastance was lower in the group receiving papain than in the group receiving saline solution, showing a functional status compatible with pulmonary emphysema, with decreased elasticity of the pulmonary tissue. Conclusion: The reproduction of an experimental model of pan-acinar pulmonary emphysema in rats was achieved by papain instillation through the respiratory tree with functional and morphologic evidences.

Keywords: Pulmonary emphysema. Experimental model. Papain. Rats. Drug instillations.

Objective: To compare the influence of two different ventilation strategies-volume-controlled ventilation (VCV) and pressure-controlled ventilation (PCV)-on the functional performance of lung grafts in a canine model of unilateral left lung transplantation using donor lungs harvested after three hours of normothermic cardiocirculatory arrest under mechanical ventilation. Methods: The study comprised 40 mongrel dogs, randomized into two groups: VCV and PCV. Of the 20 recipients, 5 did not survive the transplant, and 5 died before the end of the post-transplant assessment period. The remaining 10 survivors (5 in each group) were evaluated for 360 min after lung transplantation. The functional performance of the grafts was evaluated regarding respiratory mechanics, gas exchange, and lung graft histology. Results: There were no significant differences between the groups regarding respiratory mechanics (peak inspiratory pressure, plateau pressure, mean airway pressure, dynamic compliance, and static compliance) or gas exchange variables (PaO2, venous oxygen tension, PaCO2, venous carbon dioxide tension, and the arterial-venous oxygen content difference). The histopathological findings were consistent with nonspecific acute lung injury and did not differ between the groups. Conclusions: This model of lung transplantation showed that the functional performance of lung grafts was not influenced by the ventilation strategy employed during the first six hours after reperfusion.

Keywords: Pulmonary ventilation; Respiration, artificial; Lung transplantation; Dogs; Organ preservation.

Small animal models are particularly suitable for lung preservation studies, because they are simple and cost-effective. This brief communication focuses on the technical description of an ex vivo lung perfusion model in rats by means of a commercially available apparatus, which was the first to be installed in a thoracic surgery research laboratory in Brazil. The model and its preparation, together with its applications for lung preservation studies, are described in detail. All technical details can also be seen in a video posted on the website of the Brazilian Journal of Pulmonology.

Keywords: Lung transplantation; Reperfusion injury; Rats; Models, animal.

Objective: To evaluate the effects of azathioprine on the mucociliary system in a model of bronchial section and anastomosis in rats. Methods: Thirty-six male Wistar-Furth rats were submitted to left bronchial section and anastomosis and divided into two groups to receive either saline solution or azathioprine. After 7, 15 and 30 days of treatment, six animals from each group were killed, after which in situ mucociliary transport velocity, in vitro mucus transportability, and contact angle of mucus in the right (intact) and left (sectioned) bronchi were measured. Results: In situ mucociliary transport velocity was significantly lower in the sectioned bronchi than in the intact bronchi (p < 0.001). In situ mucociliary transport velocity was lower in the intact bronchi of the animals treated with azathioprine for 7 days (p < 0.05), and those bronchi presented full recovery after 30 days of treatment. The contact angle was higher in the mucus samples collected from the sectioned bronchi of the animals treated with saline solution for 30 days (p < 0.001), which is in accordance with the decreased in vitro mucus transportability observed in the same animals (p < 0.001). Conclusions: We conclude that, in the sectioned bronchi of rats, treatment with azathioprine causes only transitory impairment of mucociliary transport, whereas administration of saline solution impairs mucociliary transport for up to 30 days. In addition, azathioprine protects against alterations in mucus surface properties.

Keywords: Mucociliary clearance; Anastomosis, surgical; Immunosuppression; Lung.

Objective: To describe a new murine model of cigarette smoke-induced emphysema. Methods: Twenty-four male Wistar rats were divided into two groups: the cigarette smoke group, comprising 12 rats exposed to smoke from 12 commercial filter cigarettes three times a day (a total of 36 cigarettes per day) every day for 30 weeks; and the control group, comprising 12 rats exposed to room air three times a day every day for 30 weeks. Lung function was assessed by mechanical ventilation, and emphysema was morphometrically assessed by measurement of the mean linear intercept (Lm). Results: The mean weight gain was significantly (approximately ten times) lower in the cigarette smoke group than in the control group. The Lm was 25.0% higher in the cigarette smoke group. There was a trend toward worsening of lung function parameters in the cigarette smoke group. Conclusions: The new murine model of cigarette smoke-induced emphysema and the methodology employed in the present study are effective and reproducible, representing a promising and economically viable option for use in studies investigating the pathophysiology of and therapeutic approaches to COPD.

Keywords: Tobacco smoke pollution; Emphysema; Disease models, animal; Equipment and supplies.

Introduction: Surgical procedures requiring aortic occlusion have been associated with pulmonary reperfusion injury. The authors studied the pulmonary edema in a reperfusion injury model by aortic occlusion in rats. Material and methods: Thirty-three Wistar rats were anesthetized with intraperitoneal injection of sodium pentobarbital (20 mg/kg). Using a midline abdominal incision, the infra-renal aorta was isolated and the animals were randomized into three groups. Ischemia-reperfusion group (IRG, n = 5): rats that underwent 30 min of aorta occlusion and were followed during 120 min of reperfusion. Ischemia group (IG, n = 5): rats that underwent 30 min of aorta occlusion. Control group (CG, n = 5): rats that underwent sham operations without aorta occlusion and were followed during 150 min. Histopathologic examination of the right lung was performed. The pulmonary edema was studied by morphometric analysis and so was the leukocytes infiltration. Eighteen rats (6 rats in each group) were studied with respect to lung fresh/dry weight ratio. ANOVA was used to analyze the morphometric results and the lung fresh/dry weight ratio, with Bonferroni adjustment for paired multiple comparisons. Animals of the IRG presented more pulmonary edema than those of the IG and CG (0.24 vs. 0.17 and 0.17, p < 0.001). There was no difference between the groups regarding the lung fresh/dry weight ratio. There were more inflammatory cells in the lungs of the rats submitted to ischemia-reperfusion. The authors concluded that infra-renal abdominal aorta cross-clamping and unclamping are associated with pulmonary edema. This edema is not induced by elevation of the hydrostatic pressure due to the aortic occlusion, since it was not seen in animals that were only submitted to ischemia.

Keywords: ischemia, reperfusion, pulmonary edema, inbred strains rats

Objective: To develop and validate an asthma knowledge questionnaire for use in adult asthma patients in Brazil. Methods: A 34-item self-report questionnaire was constructed and administered to adult asthma patients and adult controls. The maximum total score was 34. Results: The questionnaire was shown to be discriminatory, with good reliability and reproducibility. The mean score for asthma patients and controls was, respectively, 21.47 ± 4.11 (range: 9-31) and 17.27 ± 5.11 (range: 7-28; p < 0.001). The Kaiser-Meyer-Olkin measure of sampling adequacy was 0.53, and the Bartlett's test of sphericity demonstrated a satisfactory suitability of the data to factor analysis (p < 0.001). There was no significant difference between the total scores obtained in the first and in the second application of the questionnaire within a two-week interval (p = 0.43). The internal consistency reliability (KR-20 coefficient) was 0.69. Conclusions: This study has validated an asthma knowledge questionnaire for use in Brazil.

Keywords: Asthma; Questionnaires; Validation studies; Reproducibility of results.

Objective: To present a model of prostaglandin I2 (PGI2) administration (inhaled vs. parenteral) and to assess the functional performance of the lungs in an ex vivo lung perfusion system. Methods: Forty Wistar rats were anesthetized and placed on mechanical ventilation followed by median sterno-laparotomy and anticoagulation. The main pulmonary artery was cannulated. All animals were maintained on mechanical ventilation and were randomized into four groups (10 rats/group): inhaled saline (IS); parenteral saline (PS); inhaled PGI2 (IPGI2); and parenteral PGI2 (PPGI2). The dose of PGI2 used in the IPGI2 and PPGI2 groups was 20 and 10 µg/kg, respectively. The heart-lung blocks were submitted to antegrade perfusion with a low potassium and dextran solution via the pulmonary artery, followed by en bloc extraction and storage at 4°C for 6 h. The heart-lung blocks were then ventilated and perfused in an ex vivo lung perfusion system for 50 min. Respiratory mechanics, hemodynamics, and gas exchange were assessed. Results: Mean pulmonary artery pressure following nebulization decreased in all groups (p < 0.001), with no significant differences among the groups. During the ex vivo perfusion, respiratory mechanics did not differ among the groups, although relative oxygenation capacity decreased significantly in the IS and PS groups (p = 0.04), whereas mean pulmonary artery pressure increased significantly in the IS group. Conclusions: The experimental model of inhaled PGI2 administration during lung extraction is feasible and reliable. During reperfusion, hemodynamics and gas exchange trended toward better performance with the use of PGI2 than that with the use of saline.

Keywords: Prostaglandins; Lung transplantation; Reperfusion; Models, animal; Rats.

Objective: To compare histopathological findings and the degree of apoptosis among rat lungs preserved with low-potassium dextran (LPD) solution, histidine-tryptophan-ketoglutarate (HTK) solution, or normal saline (NS) at two ischemia periods (6 h and 12 h) using an experimental rat model of ex vivo lung perfusion. Methods: Sixty Wistar rats were anesthetized, randomized, and submitted to antegrade perfusion via pulmonary artery with one of the preservation solutions. Following en bloc extraction, the heart-lung blocks were preserved for 6 h or 12 h at 4°C and then reperfused with homologous blood for 60 min in an ex vivo lung perfusion system. At the end of the reperfusion, fragments of the middle lobe were extracted and processed for histopathological examination. The parameters evaluated were congestion, alveolar edema, alveolar hemorrhage, inflammatory infiltrate, and interstitial infiltrate. The degree of apoptosis was assessed using the TdT-mediated dUTP nick end labeling method. Results: The histopathological examination showed that all of the lungs preserved with NS presented alveolar edema after 12 h of ischemia. There were no statistically significant differences among the groups in terms of the degree of apoptosis. Conclusions: In this study, the histopathological and apoptosis findings were similar with the use of either LPD or HTK solutions, whereas the occurrence of edema was significantly more common with the use of NS.

Keywords: : Organ preservation; Organ preservation solutions; Lung transplantation; Reperfusion injury; Apoptosis.

Objective: The aim of this study was to identify the best experimental model in which to observe the pulmonary alterations characterizing hepatopulmonary syndrome (HPS). Methods: Male Wistar rats, with mean weight of 250 g, were used in four experimental models: inhaled carbon tetrachloride; intraperitoneal carbon tetrachloride; partial portal vein ligation; and bile duct ligation (BDL). The animals in all groups were divided into control and experimental subgroups. The following variables were measured: transaminase levels; blood gases; lipoperoxidation, using thiobarbituric acid reactive substances (TBARS) and chemiluminescence; and levels of superoxide dismutase (SOD) anti-oxidant activity. Anatomopathological examination of the lung was also performed. Results: There were statistically significant differences between the BDL control and BDL experimental groups: aspartate aminotransferase (105.3 ± 43 vs. 500.5 ± 90.3 IU/L); alanine aminotransferase (78.75 ± 37.7 vs. 162.75 ± 35.4 IU/L); alkaline phosphatase (160 ± 20.45 vs. 373.25 ± 45.44 IU/L); arterial oxygen tension (85.25 ± 8.1 vs. 49.9 ± 22.5 mmHg); and oxygen saturation (95 ± 0.7 vs. 73.3 ± 12.07%). Lipoperoxidation and antioxidant activity also differed significantly between the two BDL groups (control vs. experimental): TBARS (0.87 ± 0.3 vs. 2.01 ± 0.9 nmol/mg protein); chemiluminescence (16008.41 ± 1171.45 vs. 20250.36 ± 827.82 cps/mg protein); and SOD (6.66 ± 1.34 vs. 16.06 ± 2.67 IU/mg protein). The anatomopathological examination confirmed pulmonary vasodilatation in the BDL model. In the other models, there were no alterations that were characteristic of HPS. Conclusions: The data obtained suggest that the BDL model can be used in future studies involving hepatic alterations related to oxidative stress and HPS.

Keywords: Hepatopulmonary syndrome; Lung; Oxidative stress; Rats.

Objective: To assess the frequency of variation in forced expiratory volume in one second after bronchodilator use in a sample of patients with chronic obstructive pulmonary disease, correlating such variation with clinical and demographic variables and evaluating the frequency of response presented in forced vital capacity, slow vital capacity, inspiratory capacity, residual volume, airway resistance and specific airway conductance. Methods: A total of 64 patients with chronic obstructive pulmonary disease were submitted to whole body plethysmography, and reversibility of bronchoconstriction after the administration 400 µg of fenoterol was quantified. Results: A response in forced expiratory volume in one second was observed in 31% of the patients. Excluding patients presenting a response in forced expiratory volume in one second, 5% presented responses in 5 of the other 6 parameters, 10% presented responses in 4 parameters, 17.5% in 3 parameters, 27.5% in 2 parameters, and 25% in only 1 parameter. Conclusion: When included in the evaluation of bronchodilator response together with forced expiratory volume in one second, static lung volumes, airway resistance and airway conductance allowed a broader evaluation of those patients presenting a functional pharmacodynamic response. These results are in accordance with the observation that bronchodilator use provides clinical improvement and relief of dyspnea to many patients with chronic obstructive pulmonary disease, even to those in whom such treatment leads to no improvement in forced expiratory volume in one second.

Keywords: Pulmonary disease, chronic obstructive/drug therapy; Bronchodilator agents/therapeutic use; Airway resistance/drug effects; Respiratory function tests; Vital capacity; Forced expiratory volume