Search

Every year, a large number of individuals become dependent on mechanical ventilation because of a loss of diaphragm function. The most common causes are cervical spinal trauma and neuromuscular diseases. We have developed an experimental model to evaluate the performance of electrical stimulation of the diaphragm in rabbits using single-channel electrodes implanted directly into the muscle. Various current intensities (10, 16, 20, and 26 mA) produced tidal volumes above the baseline value, showing that this model is effective for the study of diaphragm performance at different levels of electrical stimulation

OBJETIVO: Investigar os efeitos agudos da administração endovenosa de extrato da fumaça do cigarro (EFC) em parâmetros funcionais respiratórios, inflamatórios e histológicos em ratos e comparar esse potencial modelo de lesão pulmonar aguda (LPA) com aquele com o uso de ácido oleico (AO). MÉTODOS: Foram estudados 72 ratos Wistar machos divididos em quatro grupos: tratados somente com soro fisiológico (SF; grupo controle); tratados com EFC e SF (grupo EFC); tratados com SF e AO (grupo AO); e tratados com EFC e AO (grupo EFC/AO). RESULTADOS: As médias de complacência foram significantemente menores nos grupos AO e EFC/AO (2,12 ± 1,13 mL/cmH2O e 1,82 ± 0,77 mL/cmH2O, respectivamente) do que no controle (3,67 ± 1,38 mL/cmH2O). A proporção de neutrófilos e a atividade das metaloproteinases 2 e 9 em lavado broncoalveolar foram significantemente maiores nos grupos AO e EFC/AO que no controle. O acometimento pulmonar avaliado por morfometria foi significantemente maior nos grupos AO e EFC/AO (72,9 ± 13,8% e 77,6 ± 18,0%, respectivamente) do que nos grupos controle e EFC (8,7 ± 4,1% e 32,7 ± 13,1%, respectivamente), e esse acometimento foi significantemente maior no grupo EFC que no grupo controle. CONCLUSÕES: A administração endovenosa de EFC, nas doses e tempos deste estudo, associou-se à LPA mínima. O EFC não potencializou a LPA induzida por AO. Estudos adicionais são necessários para esclarecer o papel potencial desse modelo como método de estudo dos mecanismos de agressão pulmonar pelo tabaco.OBJECTIVE: To investigate the acute effects of intravenous administration of cigarette smoke extract (CSE) on histological, inflammatory, and respiratory function parameters in rats, as well as to compare this potential acute lung injury (ALI) model with that with the use of oleic acid (OA). METHODS: We studied 72 Wistar rats, divided into four groups: control (those injected intravenously with saline); CSE (those injected intravenously with CSE and saline); OA (those injected intravenously with saline and OA); and CSE/OA (those injected intravenously with CSE and OA). RESULTS: Mean lung compliance was significantly lower in the OA and CSE/OA groups (2.12 ± 1.13 mL/cmH2O and 1.82 ± 0.77 mL/cmH2O, respectively) than in the control group (3.67 ± 1.38 mL/cmH2O). In bronchoalveolar lavage fluid, the proportion of neutrophils was significantly higher in the OA and CSE/OA groups than in the control group, as was the activity of metalloproteinases 2 and 9. Pulmonary involvement, as assessed by morphometry, was significantly more severe in the OA and CSE/OA groups (72.9 ± 13.8% and 77.6 ± 18.0%, respectively) than in the control and CSE groups (8.7 ± 4.1% and 32.7 ± 13.1%, respectively), and that involvement was significantly more severe in the CSE group than in the control group. CONCLUSIONS: The intravenous administration of CSE, at the doses and timing employed in this study, was associated with minimal ALI. The use of CSE did not potentiate OA-induced ALI. Additional studies are needed in order to clarify the potential role of this model as a method for studying the mechanisms of smoking-induced lung injury.

OBJETIVO: Apresentar um modelo experimental de administração de prostaglandina I2 (PGI2) por via inalatória vs. parenteral e avaliar o desempenho funcional dos pulmões em um sistema de perfusão pulmonar ex vivo. MÉTODOS: Quarenta ratos Wistar foram anestesiados, ventilados, submetidos a laparotomia com ressecção do esterno e anticoagulados. O tronco da artéria pulmonar foi canulado. Todos os animais foram submetidos a ventilação mecânica. Os animais foram randomizados em quatro grupos (10 ratos/grupo): salina nebulizada (SN); salina parenteral (SP); PGI2 nebulizada (PGI2N); e PGI2 parenteral (PGI2P). A dose de PGI2 nos grupos PGI2N e PGI2P foi de 20 e 10 µg/kg, respectivamente. Os blocos cardiopulmonares foram submetidos in situ a perfusão anterógrada com solução de baixo potássio e dextrana a 4ºC via artéria pulmonar, extraídos em bloco e armazenados a 4ºC por 6 h. Os blocos foram ventilados e perfundidos em um sistema ex vivo por 50 min, sendo obtidas medidas de mecânica ventilatória, hemodinâmica e trocas gasosas. RESULTADOS: Houve redução da pressão arterial pulmonar média após a nebulização em todos os grupos (p < 0,001), sem diferença entre os grupos. Na perfusão ex vivo, a mecânica ventilatória não diferiu entre os grupos. Houve redução da capacidade relativa de oxigenação ao longo da perfusão nos grupos SN e SP (p = 0,04), e houve aumento significativo da pressão arterial pulmonar no grupo SN. CONCLUSÕES: O modelo experimental de administração de PGI2 na extração pulmonar é exequível e confiável. Na reperfusão, os resultados de hemodinâmica e de trocas gasosas demonstraram tendência a um melhor desempenho com o uso de PGI2 do que com solução salina.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 4ºC 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.

Estudos de preservação pulmonar em modelos experimentais realizados em animais de pequeno porte são de realização mais simples e barata. Esta comunicação tem o enfoque de descrever tecnicamente um modelo de perfusão pulmonar ex vivo em ratos, com o uso de um equipamento disponível comercialmente que foi o primeiro a ser instalado em um laboratório de pesquisa em cirurgia torácica no Brasil. Descrevemos detalhadamente o modelo e sua preparação, assim como suas aplicações para estudos de preservação pulmonar. Os detalhes técnicos da preparação podem ser observados também em um vídeo postado no site do Jornal Brasileiro de Pneumologia.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.

OBJETIVO: Avaliar a estabilidade das variáveis hemodinâmicas, da mecânica respiratória e de troca gasosa do modelo animal de lesão pulmonar aguda induzida por ácido oleico. MÉTODOS: Trata-se de um estudo experimental no qual foram utilizados 10 cães de raça indeterminada. As variáveis foram aferidas inicialmente e em 30, 60, 90 e 120 min após a administração do ácido oleico. Para analisar as medidas repetidas, foram testados efeitos lineares e quadráticos e foram utilizados ajustes de modelos lineares mistos com estruturas de variâncias e covariâncias diversificadas, dependendo da variável analisada. RESULTADOS: Observamos estabilidade da pressão arterial média aos 30 min, assim como da frequência cardíaca, da pressão arterial pulmonar e da pressão de capilar pulmonar aos 60 min. Frequência respiratória, volume corrente, volume minuto e trabalho respiratório estabilizaram aos 30 min. Quanto às variáveis de troca gasosa, PaO2, relação PaO2/FiO2 e fração de shunt pulmonar estabilizaram-se aos 30 min. As demais variáveis mantiveram-se em ascensão ou queda contínuas. CONCLUSÕES: O modelo de lesão pulmonar aguda induzida por ácido oleico é estável para algumas das variáveis testadas; porém, a estabilização se dá em momentos diferentes. As variáveis da mecânica respiratória e de troca gasosa estabilizaram em 30 min, e as hemodinâmicas, em 60 min.OBJECTIVE: To evaluate the stability of hemodynamic, respiratory and gas exchange variables in an animal model of oleic acid-induced acute lung injury. METHODS: This was an experimental study involving 10 mongrel dogs. The variables were measured at baseline, as well as at 30, 60, 90 and 120 min after the administration of oleic acid. In order to analyze repeated measurements, linear and quadratic effects were tested. Mixed linear models with diversified variance and covariance structures were used, depending on the variable studied. RESULTS: We found that mean arterial blood pressure stabilized at 30 min, as did heart rate, pulmonary arterial pressure and pulmonary capillary pressure at 60 min. Respiratory rate, tidal volume, minute volume and respiratory work stabilized at 30 min. Regarding gas exchange variables, PaO2, PaO2/FiO2 ratio and pulmonary shunt fraction stabilized at 30 min. The remaining variables maintained a continuous rise or fall. CONCLUSIONS: This oleic acid-induced acute lung injury model is stable for some of the variables tested, although stabilization occurs at different times. The respiratory and gas exchange variables stabilized at 30 min, whereas the hemodynamic variables stabilized at 60 min.

ABSTRACT Objective: To describe a murine model of emphysema induced by a combination of exposure to cigarette smoke (CS) and instillation of porcine pancreatic elastase (PPE). Methods: A total of 38 C57BL/6 mice were randomly divided into four groups: control (one intranasal instillation of 0.9% saline solution); PPE (two intranasal instillations of PPE); CS (CS exposure for 60 days); and CS + PPE (two intranasal instillations of PPE + CS exposure for 60 days). At the end of the experimental protocol, all animals were anesthetized and tracheostomized for calculation of respiratory mechanics parameters. Subsequently, all animals were euthanized and their lungs were removed for measurement of the mean linear intercept (Lm) and determination of the numbers of cells that were immunoreactive to macrophage (MAC)-2 antigen, matrix metalloproteinase (MMP)-12, and glycosylated 91-kDa glycoprotein (gp91phox) in the distal lung parenchyma and peribronchial region. Results: Although there were no differences among the four groups regarding the respiratory mechanics parameters assessed, there was an increase in the Lm in the CS + PPE group. The numbers of MAC-2-positive cells in the peribronchial region and distal lung parenchyma were higher in the CS + PPE group than in the other groups, as were the numbers of cells that were positive for MMP-12 and gp91phox, although only in the distal lung parenchyma. Conclusions: Our model of emphysema induced by a combination of PPE instillation and CS exposure results in a significant degree of parenchymal destruction in a shorter time frame than that employed in other models of CS-induced emphysema, reinforcing the importance of protease-antiprotease imbalance and oxidant-antioxidant imbalance in the pathogenesis of emphysema.