Administration of intrapulmonary sodium polyacrylate to induce lung injury for the development of a porcine model of early acute respiratory distress syndrome.

BACKGROUND: The loss of alveolar epithelial and endothelial integrity is a central component in acute respiratory distress syndrome (ARDS); however, experimental models investigating the mechanisms of epithelial injury are lacking. The purpose of the present study was to design and develop an experimental porcine model of ARDS by inducing lung injury with intrapulmonary administration of sodium polyacrylate (SPA). METHODS: The present study was performed at the Centre for Comparative Medicine, University of British Columbia, Vancouver, British Columbia. Human alveolar epithelial cells were cultured with several different concentrations of SPA; a bioluminescence technique was used to assess cell death associated with each concentration. In the anesthetized pig model (female Yorkshire X pigs (n = 14)), lung injury was caused in 11 animals (SPA group) by injecting sequential aliquots (5 mL) of 1% SPA gel in aqueous solution into the distal airway via a rubber catheter through an endotracheal tube. The SPA was dispersed throughout the lungs by manual bag ventilation. Three control animals (CON group) underwent all experimental procedures and measurements with the exception of SPA administration. RESULTS: The mean (± SD) ATP concentration after incubation of human alveolar epithelial cells with 0.1% SPA (0.92 ± 0.27 μM/well) was approximately 15% of the value found for the background control (6.30 ± 0.37 μM/well; p < 0.001). Elastance of the respiratory system (E RS) and the lung (E L) increased in SPA-treated animals after injury (p = 0.003 and p < 0.001, respectively). Chest wall elastance (E CW) did not change in SPA-treated animals. There were no differences in E RS, E L, or E CW in the CON group when pre- and post-injury values were compared. Analysis of bronchoalveolar lavage fluid showed a significant shift toward neutrophil predominance from before to after injury in SPA-treated animals (p < 0.001) but not in the CON group (p = 0.38). Necropsy revealed marked consolidation and congestion of the dorsal lung lobes in SPA-treated animals, with light-microscopy evidence of bronchiolar and alveolar spaces filled with neutrophilic infiltrate, proteinaceous debris, and fibrin deposition. These findings were absent in animals in the CON group. Electron microscopy of lung tissue from SPA-treated animals revealed injury to the alveolar epithelium and basement membranes, including intra-alveolar neutrophils and fibrin on the alveolar surface and intravascular fibrin (microthrombosis). CONCLUSIONS: In this particular porcine model, the nonimmunogenic polymer SPA caused a rapid exudative lung injury. This model may be useful to study ARDS caused by epithelial injury and inflammation

Avaliação da pressão inspiratória máxima em pacientes críticos não-cooperativos: comparação entre dois métodos

CONTEXTUALIZAÇÃO: A ventilação mecânica, embora necessária para o tratamento da insuficiência respiratória aguda, pode estar associada ao descondicionamento e à disfunção muscular respiratória. A avaliação da pressão inspiratória máxima (PiMáx) é utilizada para estimar a força muscular inspiratória de pacientes ventilados artificialmente, porém não há uma definição quanto à melhor forma de realizar esta medida. OBJETIVO: Comparar 2 métodos de avaliação da PiMáx, por meio de 4 protocolos diferentes, em pacientes não cooperativos ventilados artificialmente. MÉTODO: Foram avaliados 30 pacientes não cooperativos e em processo de desmame da ventilação mecânica. De acordo com a randomização em blocos, o Método de Oclusão Simples (MO) e o Método da Válvula Unidirecional (VU) foram aplicados com tempo de duração de 20 e 40 segundos para cada paciente. Adicionalmente, durante as medições em 40s, foi anotado o valor da PiMáx em 30s. RESULTADOS: Os valores de PiMáx foram maiores em 40s do que em 20s para MO (48,2 ± 21,7 vs 36 ± 18,7 cmH2O; p< 0,001) e VU (56,6 ± 23,3 vs 43,4 ± 24 cmH2O; p< 0,001). Os valores de PiMáx foram maiores no método VU em 40s (VU40) do que MO em 40s (MO40) (56,6 ± 23,3 vs 48,2 ± 21,7 cmH2O; p< 0,001). Houve diferença entre VU em 30 e 40s (51,5 ± 20,8 vs 56,6 ± 23,3 cmH2O; p< 0,001). CONCLUSÃO: Em pacientes não-cooperativos, valores maiores de PiMax são obtidos com o método da válvula unidirecional com oclusão durante 40 segundos em comparação com os outros protocolos avaliados