Pesquisa, um dos pilares da história do HCPA

O ano de 2011 vem proporcionando importantes resgates históricos no âmbito do Hospital de Clínicas de Porto Alegre. Aproveitando o ensejo da comemoração de seu 40º aniversário, a Instituição dedica-se a recuperar a memória de episódios e personagens importantes em sua rica e bem-sucedida trajetória

Lung transplantation in cystic fibrosis

A progressão do acometimento pulmonar e a evolução para insuficiência respiratória são responsáveis por importante morbimortalidade em pacientes com fibrose cística. O transplante pulmonar está consolidado como tratamento de escolha para diversas pneumopatias em estágios terminais e vem sendo realizado em pacientes com fibrose cística avançada desde a década de 1980. A seleção de pacientes candidatos ao transplante envolve a análise cuidadosa de parâmetros clínicos, fisiológicos e laboratoriais, com atenção a fatores conhecidos de mau prognóstico como: piora acentuada e acelerada da função pulmonar, aumento da frequência e gravidade das exacerbações, desnutrição, diabetes melito, hemoptise volumosa, pneumotórax, hipoxemia e hipercapnia em ar ambiente, hipertensão pulmonar e distância reduzida no teste de caminhada de seis minutos. Embora o tema ainda gere controvérsias, a maioria dos centros transplantadores contraindica o transplante para portadores de Burkholdelia cepacia. A presença de outros germes colonizantes no escarro, ainda que com perfil adverso de sensibilidade aos antibióticos, não costuma impedir a realização do transplante em pacientes com fibrose cística. A avaliação pré-transplante nesta população segue os mesmos padrões das demais indicações, com atenção especial ao suporte nutricional, ao perfil microbiológico e à evolução recente do contexto clínico global e da função pulmonar. Os resultados do transplante pulmonar bilateral na fibrose cística são em regra superiores aos das demais indicações.Progressive involvement of the lungs and the development of respiratory failure are major causes of morbidity and mortality in patients with cystic fibrosis. Lung transplantation is a well-established treatment for several end-stage respiratory diseases and it has been successfully performed in cystic fibrosis patients since the 1980’s. Patient selection involves careful analysis of clinical, physiologic and laboratorial parameters, with special consideration of well-known adverse prognostic factors such as: accelerated loss of lung function, increase in frequency and severity of exacerbations, poor nutritional status, diabetes mellitus, massive hemoptysis, pneumothorax, hypoxemia and hypercapnia while breathing room air, pulmonary hypertension, and reduced distance in the 6-minute walk test. Despite some controversy, most transplant centers refuse patients with Burkholderia cepacia for transplantation. Other colonizing pathogens, even with extensive antibiotic resistant patterns, do not, in general, preclude the procedure in patients with cystic fibrosis. Pre-transplant evaluation of this population is similar for other indications, with special attention to nutritional support, microbiological profile analysis and recent changes of the clinical context and lung function. The results of bilateral lung transplantation for cystic fibrosis are generally better than for other indications

Chest wall hemangioma : a difficult preoperative diagnosis

We report a case that presents a diagnostic challenge in a 22 year-old female. CT-Scan and MRI showed a soft-density mass (12 cm) causing middle arch erosion of the fifth rib. In this rapidly-growing chest wall tumor a surgical-biopsy was very hemorrhagic and frozen section was unabled to disclose a sarcoma. Angiography and embolization of the feeding arteries were done. The final histopathology pointed out hemangioma. Complete resection was performed without prosthesis interposition. We emphasize two points regarding vascular chest wall tumors: (1) its possibility to mimick a sarcoma, so the surgical planning demands preoperative diagnosis; (2) the positive role of embolization in large and fast-growing lesions

Development of different degrees of elastaseinduced emphysema in mice : a randomized controlled experimental study

Introduction: Mouse models of emphysema are important tools for testing different therapeutic strategies. The aim of this study was to develop a mouse model of emphysema induced by different doses of elastase in order to produce different degrees of severity. Methods: Thirty female mice (C57BL/6) were used in this study. Different doses of porcine pancreatic elastase were administered intratracheally once a week for four weeks, as follows: 0.1 U (n=8), 0.15 U (n=7), and 0.2 U (n=7). Control mice (n=8) received 50 microL of sterile saline solution intratracheally. Lung mechanics were analyzed by plethysmography. Mean linear intercept and volume fraction occupied by collagen and elastic fibers were determined. Results: An increase in lung resistance was observed with 0.2 U of elastase [median (P-25-P75): 2.02 (1.67; 2.34) cmH2O.s/mL], as well as a decrease in tidal volume and minute ventilation. Peak expiratory flow increased significantly in the groups treated with 0.15 U and 0.2 U of elastase. Mean linear intercept was higher with 0.15 U and 0.2 U of elastase, with destruction of alveolar walls [median (P-25-P75): 30.31 (26.65-43.13) microm and 49.49 (31.67-57.71) microm respectively]. The volume fraction occupied by collagen and elastic fibers was lower in the group receiving 0.2 U of elastase. Conclusion: Four intratracheal instillations of 0.2 U of elastase once a week induced changes in lung function and histology, producing an experimental model of severe pulmonary emphysema, whereas 0.15 U resulted in only histological changes

Development of different degrees of elastase-induced emphysema in mice: a randomized controlled experimental study

Introduction: Mouse models of emphysema are important tools for testing different therapeutic strategies. The aim of this study was to develop a mouse model of emphysema induced by different doses of elastase in order to produce different degrees of severity.Methods: Thirty female mice (C57BL/6) were used in this study. Different doses of porcine pancreatic elastase were administered intratracheally once a week for four weeks, as follows: 0.1 U (n=8), 0.15 U (n=7), and 0.2 U (n=7). Control mice (n=8) received 50 microL of sterile saline solution intratracheally. Lung mechanics were analyzed by plethysmography. Mean linear intercept and volume fraction occupied by collagen and elastic fibers were determined.Results: An increase in lung resistance was observed with 0.2 U of elastase [median (P-25-P75): 2.02 (1.67; 2.34) cmH2O.s/mL], as well as a decrease in tidal volume and minute ventilation. Peak expiratory flow increased significantly in the groups treated with 0.15 U and 0.2 U of elastase. Mean linear intercept was higher with 0.15 U and 0.2 U of elastase, with destruction of alveolar walls [median (P-25-P75): 30.31 (26.65-43.13) microm and 49.49 (31.67-57.71) microm respectively]. The volume fraction occupied by collagen and elastic fibers was lower in the group receiving 0.2 U of elastase.Conclusion: Four intratracheal instillations of 0.2 U of elastase once a week induced changes in lung function and histology, producing an experimental model of severe pulmonary emphysema, whereas 0.15 U resulted in only histological changes.Introduction: Mouse models of emphysema are important tools for testing different therapeutic strategies. The aim of this study was to develop a mouse model of emphysema induced by different doses of elastase in order to produce different degrees of severity. Methods: Thirty female mice (C57BL/6) were used in this study. Different doses of porcine pancreatic elastase were administered intratracheally once a week for four weeks, as follows: 0.1 U (n=8), 0.15 U (n=7), and 0.2 U (n=7). Control mice (n=8) received 50 microL of sterile saline solution intratracheally. Lung mechanics were analyzed by plethysmography. Mean linear intercept and volume fraction occupied by collagen and elastic fibers were determined. Results: An increase in lung resistance was observed with 0.2 U of elastase [median (P-25-P75): 2.02 (1.67; 2.34) cmH2O.s/mL], as well as a decrease in tidal volume and minute ventilation. Peak expiratory flow increased significantly in the groups treated with 0.15 U and 0.2 U of elastase. Mean linear intercept was higher with 0.15 U and 0.2 U of elastase, with destruction of alveolar walls [median (P-25-P75): 30.31 (26.65-43.13) microm and 49.49 (31.67-57.71) microm respectively]. The volume fraction occupied by collagen and elastic fibers was lower in the group receiving 0.2 U of elastase. Conclusion: Four intratracheal instillations of 0.2 U of elastase once a week induced changes in lung function and histology, producing an experimental model of severe pulmonary emphysema, whereas 0.15 U resulted in only histological changes